Tuning The Engine of Cognition
Tuning The Engine of Cognition
Tuning The Engine of Cognition
cortex
Abstract
The prefrontal cortex of the primate frontal lobes provides the capacity for judgment which
can constantly adapt behavior in order to optimize its outcome. Adjudicating between long-
term memory programs and prepotent responses, this capacity reviews all incoming
information and provides an interpretation dependent on the events that have just occurred,
the events that are predicted to happen, and the alternative response strategies that are
available in the given situation. It has been theorized that this function requires two essential
integrated components, a central executive which guides selective attention based on
mechanisms of associative memory, as well as the second component, working memory
buffers, in which information is held online, abstracted, and translated on a mental sketchpad
of work in progress. In this review, we critically outline the evidence that the integration of
these processes and, in particular, the induction and maintenance of persistent activity in
prefrontal cortex and related networks, is dependent upon the interaction of dopamine D1 and
glutamate NMDA receptor signaling at critical nodes within local circuits and distributed
networks. We argue that this interaction is not only essential for representational memory, but
also core to mechanisms of neuroadaptation and learning. Understanding its functional
significance promises to reveal major new insights into prefrontal dysfunction in
schizophrenia and, hence, to target a new generation of drugs designed to ameliorate the
debilitating working memory deficits in this disorder.
Article Outline
Critical insights into the cellular substrates subserving working memory in PFC have come
from studies of neuronal activity in nonhuman primates performing delayed response tasks.
As first demonstrated by Kubota and Niki (1971) in delayed alternation and by Fuster and
Alexander (1971) in spatial delayed response, neurons in primate DLPFC appear to encode
the location of a target in space that is used to guide a response at the end of the delay period
in the task. At around the same time that recording in delayed response originated in PFC,
Wurtz and Goldberg (1972) discovered neurons in the superior colliculus that responded prior
to saccade initiation in an oculomotor task. When this was examined in FEF, a critical node
in the network involved in control of eye movements, neurons were found in this region
whose firing anticipated a forthcoming saccade during a delay period (Bruce & Goldberg,
1985). At one and the same time, applying the ODR task to the study of DLPFC function and
recognizing that neuronal activity during delayed response tasks was representative of
working memory, Goldman-Rakic (1987) and colleagues (Funahashi et al., 1989, Funahashi
et al., 1990 and Funahashi et al., 1991) were able to reveal the cellular substrate of working
memory and multiple neuronal processes involved (Goldman-Rakic, 1990). Thus, it was
found that neurons in Areas 46 and 8a, in the region of the caudal principal sulcus, showed
spatially tuned delay activity, or ―memory fields‖ with particular neurons encoding selective
target locations by firing maximally for preferred directions and minimally for nonpreferred
directions of the opposite region in the visual field. Neurons bearing memory fields
frequently also show responses to the sensory stimulus itself (cue activity) and the initiation
of the saccadic response (presaccadic activity), while other neurons show such cue and/or
presaccadic responses without mnemonic activity. Thus, multiple aspects of working memory
appear to be encoded by prefrontal neurons which enable the transitions from sensory
information through a transient storage process to guidance of the appropriate response. In
the monkey, it was shown that the delay activity remained reasonably accurate in guiding
saccades over delays of five or more seconds (Funahashi et al., 1989), an indication perhaps
that the persistent activity of particular neurons could maintain neural representation of a
stimulus over meaningful periods of behavior consistent with the fMRI findings of Leung et
al. (2002). Given the impact of multiple neuropsychiatric and neurological disorders, such as
schizophrenia or Parkinson‘s Disease (PD) on working memory, the ability to generate
persistent activity, while maintaining its spatial tuning, has become one of the most critical
issues for neuroscience research. As the principal neurons of PFC are pyramidal cells, it
might be expected that these neurons bear primary responsibility for working memory
processing. In fact, fast-spiking, putative interneurons in this region bear very similar
functional characteristics to their neighboring pyramidal cells exhibiting isodirectional tuning
of cue, delay, and presaccadic responses (Rao, Williams, & Goldman-Rakic, 1999). Thus, it
is evident that it is not only excitatory components arising from connections between
pyramidal cells, but also inhibitory components arising from GABAergic interneurons that
are involved in the neural circuitry that generates and maintains spatially tuned delay activity.
As we will discuss here, the significance of the NMDA contribution to the excitatory
components (Lisman et al., 1998 and Wang, 1999) and dopaminergic modulation of both
components (Durstewitz, Seamans, & Sejnowski, 2000a) appear to be critical to our
understanding of prefrontal function in working memory as well as its disruption in mental
disorders.
Studies in the nonhuman primate, using a wide variety of experimental manipulations, have
established a critical role for dopamine in working memory particularly in relation to
prefrontal function. The importance of dopamine in this region was first demonstrated in a
seminal study by Brozoski and colleagues (1979). 6-Hyroxydopamine (6-OHDA) lesions of
DLPFC produced a profound delay-dependent deficit in delayed alternation performance of
nonhuman primates that was ameliorated by subsequent administration of levodopa (l-dopa).
In the nonhuman primate, repeated administration of the dopaminergic neurotoxin 1-methyl-
4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been employed to model the core symptoms
of PD including both motoric and cognitive deficits (e.g., Kolata, 1983 and Langston et al.,
1984). Interestingly, while low dose MPTP treatment produces persistent deficits in working
memory, it results in only transient motor symptoms reminiscent of the disorder (Fernandez-
Ruiz et al., 1995, Fernandez-Ruiz et al., 1999, Schneider and Roeltgen, 1993, Schneider et
al., 1994a, Schneider et al., 1994b, Schneider and Pope-Coleman, 1995, Schneider et al.,
1999 and Schneider et al., 2003). Similar to the findings for 6-OHDA, acute administration of
l-dopa effectively alleviates deficits in working memory, as measured by performance on the
spatial delayed response task, in MPTP-treated nonhuman primates (Fernandez-Ruiz et al.,
1999). In humans, studies of PD patients on and off l-dopa have also pointed to a critical role
for dopamine in PFC for successful performance of spatial working memory tasks. Lange and
colleagues (1992) first demonstrated that withdrawal from l-dopa replacement therapy for
more than 13 h in PD patients induced deficits in spatial working memory which were
reversed one hour after reinstatement of treatment. Moreover, findings from imaging studies
have shown that l-dopa treatment in patients with PD serves both to normalize regional
cerebral blood flow (rCBF) and to focus (BOLD) the extent of prefrontal cortical activation
recruited during a working memory task (Cools et al., 2002 and Mattay et al., 2002). This
restitution of normal prefrontal function was found to be correlated with a reduction in errors
as compared to the same patients 12 h off l-dopa in the fMRI study, but was also manifested
despite no significant deficit compared to controls in the rCBF study. Taken together, these
findings were amongst the first to indicate that (i) a minimum level of dopamine transmission
is required in DLPFC for cellular mechanisms in this region to function normally, and (ii)
pharmacologically induced elevations of dopamine signaling above this level may further
improve prefrontal function sufficiently to enhance spatial working memory performance:
i.e., elevations in dopamine signaling can have ―cognitive-enhancing‖ actions. Further
insights into the essential role for dopamine in PFC in working memory stem from recent
research on genotypic variations such as the met/val polymorphism of the gene encoding
catechol-O-methyltransferase (COMT) which is thought to influence the prevailing level of
dopamine in PFC. Substitution of valine for methionine in this gene results in augmented
catabolism of dopamine and hence, reduced dopaminergic transmission (Weinberger et al.,
2001). As might be predicted from the above findings from lesion and PD studies, individuals
with greater load of the val allele demonstrated a greater extent of cortical recruitment
visualized by the BOLD signal with increasing working memory load. This sign of
potentially reduced efficiency of prefrontal function as measured by fMRI was associated
with worse performance in comparison with subjects carrying a higher load of the met allele
(Egan et al., 2001 and Goldberg et al., 2003). In accord with these findings, amphetamine
(AMPH) administration has been shown to reduce cortical efficiency at the highest memory
load in the N-back task, a test of working memory capacity, in subjects with the met/met
genotype (Mattay et al., 2003) and coincidence of this genotype with the dopamine
transporter (DAT) 10 repeat allele yields the most focused BOLD response in subjects
performing a working memory task (Bertolino et al., 2006). Given this evidence for the
influence of prevailing dopamine levels on the putative indices of efficiency of prefrontal
cortical function, it has been postulated that dopaminergic transmission may modulate
neuronal circuitry in this region in a manner which augments signal while attenuating noise.
This hypothesis has been supported by the findings of Winterer et al. (2006) which showed
that both PFC and associated neural circuitry carry diminished signal and elevated noise in
subjects with the val/val genotype performing an oddball task that recruits these regions.
Fig. 2. Mean percent correct performance on spatial delayed response is shown for two aged
female rhesus monkeys across test sessions for seven different experimental treatment
conditions including baseline (a), chronic escalating doses of haloperidol up to
0.35 mg/kg/day (b), repeated, intermittent coadministration of ABT-431 (0.00001 interleaved
with 0.0001 mg/kg; IM 30 min. prior to cognitive testing; see Castner et al., 2000a and
Castner and Goldman-Rakic, 2004 for details) (c), post-D1 testing period with continued
administration of haloperidol (d), performance at approximately 1 year post D1 treatment (e),
reinstatement of cognitive enhancement under continued haloperidol treatment by replicating
the original D1 agonist regime (f), and performance across sessions after completion of the
second round of D1 therapy under continued haloperidol administration (g). Animals
performed at a stable baseline prior to chronic administration of haloperidol, until a dose of
0.35 mg/kg of haloperidol was administered upon which performance deteriorated rapidly.
Adjuvant D1 therapy progressively improved performance to their original baseline level and
performance remained stable until approximately 1 year after starting the first D1 regime,
despite continued administration of haloperidol. Around 1 year, performance of these two
animals was consistently lower than baseline. Thus, the D1 regime was repeated a second
time which resulted again in a significant reinstatement of cognition to levels above baseline
performance and this improved performance was maintained out to several months after
cessation of the adjuvant D1 treatment.
Stemming from its pronounced effects on PFC in humans, its potential viability as a model
relevant to schizophrenia, and its potential for abuse, the acute ketamine model has been
exploited in nonhuman primates to further investigate its putative deleterious consequences
for cognition. Taffe, Davis, Gutierrez, and Gold (2002b) found that acute ketamine (1.0–
1.78 mg/kg) administration impaired the performance of rhesus monkeys on tasks designed to
test working memory and visual recognition memory, serial self-ordered spatial search and
delayed match-to-sample, respectively. These investigators have further confirmed that acute
ketamine induces deficits in recognition memory by testing monkeys under the same
paradigm on a task requiring visuo-spatial paired-associates learning (Taffe, Weed, Gutierrez,
Davis, & Gold, 2002a). Further evidence for the utility of acute ketamine to model cognitive
symptoms akin to those found in patients with schizophrenia comes from the work of Stoet
and Snyder (2006) where they demonstrated that acute ketamine administration in monkeys
not only impairs overall accuracy but also the animals ability to ignore task irrelevant stimuli
on a Stroop-like task. Moreover, using an oculomotor paradigm, Condy, Wattiez, Rivaud-
Pechoux, and Gaymard (2005) showed that acute ketamine impairs performance on an
antisaccade task in nonhuman primates by increasing error rate and antisaccade latency—
deficits similar to those found in patients with schizophrenia. In ongoing studies in our
laboratory, we have found that acute ketamine profoundly impairs spatial working memory
performance of young adult rhesus monkeys, as assessed by spatial delayed response
(Roberts et al. Society for Neuroscience Astracts 2006). The acute nature of the deficits
induced and its parallel to those in humans make this an ideal model for evaluating potential
novel cognitive enhancers designed to target cognitive deficits in patients with schizophrenia.
One potential manifestation of the synergistic action on sustained synaptic inputs between D1
and NMDA receptor stimulation is the generation of up-states as originally described in
striatum and then PFC (Lewis and O‘Donnell, 2000, West and Grace, 2002 and Wilson and
Kawaguchi, 1996). Periods of up-states, as measured by a relative depolarization of neurons
over a period of hundreds of milliseconds, are associated with periods when the cell shows
increased excitability to its excitatory inputs. It has been hypothesized that these up-states are
generated by a combination of recurrent excitatory and inhibitory inputs arising within local
circuits (McCormick et al., 2003 and Shu et al., 2003). In tandem with the depolarization,
synaptic barrages and noise can contribute to an increased probability of firing. As such the
up-states provide a functional substrate for persistent activity which can be rapidly initiated
and terminated by specific synaptic inputs to the neuron. Lewis and O‘Donnell (2000) have
shown that stimulation of the ventral tegmental area (VTA) containing mesocortical
dopamine neurons (Thierry, Blanc, Sobel, Stinus, & Golwinski, 1973) in the rodent had
differential effects upon prefrontal cortical activity dependent upon the presence of up-states
in the neurons. When burst firing was simulated by a train of stimulation in the VTA, a long-
lasting switch of membrane potential to the up-state was observed which could be blocked by
a D1 receptor antagonist. Moreover, oscillations in local field potentials of the VTA are
synchronized with up-states in PFC and transient block of VTA activity leads to disruption of
up-states and loss of LFPs in PFC (Peters, Barnhardt, & O‘Donnell, 2004). These findings
suggest that there is a critical relation between the local circuits generating up-states in PFC
and their dopaminergic modulation arising from the mesencephalon. In addition to these
findings, Seamans and colleagues (Lavin et al., 2005) have suggested that there are two
modes by which dopamine neuron firing may have an influence on up-states and the
excitability of neurons in PFC. The first is the generation of a fast postsynaptic potential
postulated to be mediated by glutamate and the second is a long-term potentiation of firing in
response to transient dopamine release. Since the phasic firing of dopamine neurons has been
hypothesized to reflect a temporal prediction error in reward (Hollerman & Schultz, 1998),
these findings were used to suggest that the fast inputs arising from glutamate may reflect a
salient signal whereas the prolonged modulation of firing may reflect a state-dependent
change in prefrontal cortical circuitry. While these predictions provide a fascinating new
route for investigating prefrontal function, it must be recognized that VTA stimulation is not
synonymous with temporal reward prediction error and that prefrontal cortical circuitry in the
absence of a demanding cognitive process may lack specific glutamatergic excitatory inputs
which may be normally make a substantial contribution for promoting transitions to increased
excitability in the functional organism. Thus, it remains an open question as to whether the
phasic firing of dopamine neurons contributes to a salience-related signal in PFC. In striatum,
the phasic firing of dopamine neurons resulting from stimulation of the median forebrain
bundle for periods as brief as 125ms (yielding just 6 cycles of a sinusoidal stimulation) can
invoke a robust phasic peak of firing in striatal neurons (Williams and Millar, 1990a and
Williams and Millar, 1990b). Similar activation of striatal neurons by phasic MFB
stimulation has been shown to be highly attenuated by systemic administration of a D1
antagonist (Gonon, 1997). Thus, it is proposed here that synergism between dopaminergic
and glutamatergic inputs arriving on prefrontal neurons in relation to the onset of a stimulus
requiring working memory processing is a vital component in the generation of persistent
activity that can subserve the neural representation of the stimulus, dependent on context. In
other words, we suggest that there is normally a phasic dopamine input on to PFC cells that
enables NMDA receptor dependent transitions in to a state of increased excitability which
promotes mnemonic activity. In this model, co-release of glutamate from dopaminergic
neurons would be anticipated to increase the cell‘s responsiveness to the immediately
following dopamine receptor activation and the dopamine release itself would lead to
synergistic support of activation resulting from sufficiently strong and cohesive sensory
inputs and promotion of any ensuing persistent activity that is NMDA-dependent. However,
just as transition to up-states can be switched on or off at any second, and just as attention to
any stimulus can be relevant at one moment and irrelevant the next, the D1 support of
NMDA transmission is temporally constrained such that it can be terminated by specific
synaptic inputs. One illustration of how this might work is the ODR task itself, where
illumination of the central fixation stimulus does not accurately predict the timing of
reinforcement at the end of the trial since the animal can take varying periods of time to
actually fixate on the stimulus. However, illumination of the peripheral cue stimulus does
provide this temporal prediction, which is contingent on its association in long term memory
with a learned motor response—a saccade—to the remembered target location. This phasic
response of dopamine neurons would be predicted from the findings of Schultz and
colleagues (1993) who investigated conditioned and unconditioned dopamine neuron activity
in the acquisition of a delayed response task. Moreover, results from the same study also
predict some conditional firing of dopamine neurons in response to the extinction of the
fixation stimulus at the end of the delay period, as this acts as a ―Go‖ signal for the animal to
make the appropriate saccade, and which therefore closely predicts time to reinforcement. As
noted by Schultz and colleagues, dopamine neurons do not show elevated or burst firing
during the delay period itself which indicates (1) that dopamine neuron firing is particularly
important to the initiation of persistent activity and (2) that the supposition by Seamans et al.
that phasic activation of dopamine neurons produces a prolonged change in state of PFC local
circuits may equate to a dopamine-mediated support of delay activity subsequent to phasic
dopamine release. Indeed, the firing induced by phasic stimulation has been shown to result
in activation of striatal neurons for several seconds in the anesthetized rat (Gonon, 1997 and
Williams and Millar, 1990a).
In liaison with orbitofrontal cortex, the anterior cingulate cortex (ACC) also plays a critical
role in monitoring outcome but one that is more tuned to the assessment of whether a
particular response is appropriate, given the expectation of reward in a particular context (see
Rushworth, Walton, Kennerle, & Bannerman, 2004, for review). This role has been
postulated to involve a signaling of the degree of conflict between the response being made
and the likelihood of obtaining the best outcome (Carter, Botvinick, & Cohen, 1999). An
alternative, but not entirely distinct hypothesis is that ACC is a central node in the circuitry
used for error detection, as manifested by the error-related negative potential (ERN; Gehring
& Fencsik, 2001). In this respect, ERN recorded by scalp electrodes has been shown to be
abnormally low in patients with schizophrenia, despite abnormally large potentials related to
commission of correct responses and evidence from other potentials of error awareness
(Alain et al., 2002 and Mathalon et al., 2002). Holroyd and Coles (2002) were among the first
to develop a computational model for the generation of the ERN which includes the input
from the reward prediction error provided by the mesocortical dopamine system. It is
therefore of interest to note that a significantly reduced ERN has been found in otherwise
high functioning elderly subjects, and this may be directly explained from the model by an
attenuation in the phasic firing of dopamine neurons (Nieuwenhuis et al., 2002). Consistent
with this hypothesis, Zirnheld et al. (2004) have shown that haloperidol administration can
lead to an impairment in learning associated with a reduction in ERN. As yet, there are no
direct data on the role of NMDA transmission in the functions of ACC; however, as shown
by Vollenweider et al., 1997a and Vollenweider et al., 1997b, ketamine induces increased
metabolic activity of ACC in healthy human subjects in association with induction of
psychosis-like symptoms (see also Rowland et al., 2005b). It has also been found that
ketamine-induced increases in rCBF in ACC in patients with schizophrenia which show an
acute exacerbation of their psychotic symptoms in response to the drug (Lahti et al., 1995 and
Holcomb et al., 2005). Moreover, the ketamine-induced psychosis-like symptoms in healthy
human volunteers are negatively correlated with dopamine efflux in ACC and DLPFC, as
measured by D2/D3 radioligand binding, despite the fact that there is no significant change in
the level of dopamine release in these regions (Aalto et al., 2005). This result would not be
predicted from a D2 antagonist—typical antipsychotic—approach to treatments of symptoms,
particularly those exacerbated by ketamine administration. Thus, it is interesting to note that
patients withdrawn from antipsychotic medication for 3 weeks or more show a significant
increase in metabolism in ACC (Holcomb et al., 1996 and Miller et al., 1997). High
frequency trains of stimulation to the VTA in the rat have been shown to produce a transition
in membrane potential to prolonged depolarization and a frequency-dependent intense
persistent firing in ACC neurons (Onn & Wang, 2005). This effect was attenuated by
systemic administration of a D1 agonist and abolished by acute dopamine depletion,
indicating an important role for dopamine receptor stimulation, particularly of the D1 family
subtype, for this activation of ACC. Taken together, these findings indicate that there is an
interaction between D1 and NMDA receptor function at the level of ACC which is likely to
have a substantial impact on central executive and working memory functions, in close
relation to DLPFC. Specific studies are required to determine the extent to which local
interactions between D1 and NMDA receptor transmission influence the error and conflict-
related processes in this region.
While the evidence for a critical interaction of NMDA and D1 receptors on cortical neuronal
activity is well substantiated, it remains to be determined as to how this interaction leads to
selective mnemonic activity that is highly tuned to the information being represented. To
better understand this issue, it is important to recognize that the influence on the activity of
both pyramidal cells and interneurons must operate in a concerted manner based on local
circuit function within PFC and the extrinsic circuits/networks with which it communicates.
Within the local circuits themselves, there are functional nodes related to cell phenotype and
structural components related to radially arranged aggregations of neurons and their dendrites
as well as the afferents/efferents that they receive. Beginning with the major cellular
phenotype, there are multiple aspects of D1 receptor modulation which can interact with both
NMDA signaling and the depolarization state of pyramidal cells. A number of these aspects
were first described by Yang and Seamans (1996) for layer V pyramidal cells. These
researchers showed that dopamine acting via D1 receptors facilitated EPSPs in these cells and
potentiated L-type calcium channel conductances, while at the same time attenuating N- and
P-type calcium conductances primarily associated with inputs from distal dendrites on to the
apical trunk. Surmeier and colleagues (1995) were able to confirm this D1 modulation of
calcium ion channels in rat neostriatal neurons, and demonstrated that the D1 modulation of
L-type channel conductances in these cells facilitates their firing provided the cells were at a
sufficiently depolarized membrane potential (Hernandez-Lopez, Bargas, Surmeier, Reyes, &
Galarraga, 1997). Thus, increased NMDA channel opening with membrane depolarization
can be indirectly supported by the D1 receptor influence on calcium conductance. In addition,
a dopamine D1-mediated potentiation of the persistent inward sodium conductance (INaP)
which can normally facilitate firing in these neurons has been identified obtained in slices
from rat PFC (Gorelova and Yang, 2000 and Yang and Seamans, 1996). However, this
finding was not observed in acutely isolated rat PFC neurons and it remains to be seen if this
enhancement of INaP by D1 stimulation depends on indirect or as yet unknown signaling
mechanisms that may not be present in an isolated neuron preparation (Maurice, Tkatch,
Meisler, Sprunger, & Surmeier, 2001). From their observations, Yang and colleagues (1999)
posited a model of how D1 modulation tunes the signal throughput of pyramidal cells in layer
V and how this tuning might be altered in schizophrenia. In this model, D1 stimulation would
facilitate those EPSPs arriving at the soma and increase the likelihood to reach threshold for
spiking such that for any given input to this region D1 stimulation would produce a greater
output, with presumably a greater frequency response for the neuron. At the same time, they
proposed a filtration mechanism which acts in conjunction with the signal amplification
process. They describe this filter as mediated by the attenuation of calcium influx through
high threshold calcium ion channels, gating inputs from the distal dendrites. The significance
of this filter would then be that original excitatory inputs from afferents to the distal dendrites
would have to be sufficiently strong (and presumably summative) in order to undergo
amplification in the perisomatic region. Such a filtration mechanism could be posited to be
more selective to inputs on a particular dendritic branch or more widespread inputs to the
distal dendrites in general. On the other hand, it could also be posited to be preferentially
selective for inputs where there is a strong association between D1 and NMDA receptors and
where AMPA receptors may be more abundant on postsynaptic sites. Thus, the trapping of
D1 receptors in the neck of dendritic spines could be important for this selection (Scott et al.,
2006). In addition, the functional recruitment of AMPA receptors to the membrane would
also contribute to this effect.
This possibility has been revealed by a recent study in primary cultures of rat PFC neurons in
which it was found that D1 stimulation results in trafficking of GluR1-containing AMPA
receptors to the membrane surface via a PKA-dependent mechanism (Sun, Zhao, & Wolf,
2005). However, it was only with subsequent NMDA receptor stimulation that GluR1
subunits became translocated into synapses from an extrasynaptic pool. Thus, a conjunction
of signaling through the D1 and NMDA receptors can lead to additional signaling from
afferent inputs to PFC pyramidal cells which enables fast synaptic transmission. This
particular aspect of the interaction between D1 and NMDA receptors highlights an important
role in a powerful mechanism of synaptic plasticity, one we shall come back to later when we
discuss the relevance of the interaction to learning and neuroadaptive processes in the brain.
We are currently studying in vivo mechanisms that may support the in vitro evidence for a
functional filtration of glutamatergic inputs to prefrontal pyramidal cells. The in vitro data
described above suggest that elevations of D1 receptor stimulation would attenuate firing that
results from glutamatergic inputs on to distal dendrites. We have directly tested this
mechanism of modulation by iontophoretic application of D1 agonists and antagonists in a
cyclic manner, interleaved with brief (5 s) pulses of glutamate application. As shown in the
example of Fig. 4, the periodic pulsatile application of glutamate induces brief bursts of
spiking in pyramidal cells which are reasonably consistent over time. Upon interleaved
application of the D1 agonist, A77636, there is a delayed, but robust, attenuation of the
glutamate-evoked activity which persists long after cessation of D1 agonist application (top
panel). Conversely, in another neuron in which the same pulsatile glutamate application was
tested (bottom panel), interleaved iontophoresis of the D1 antagonist, SCH39166, actually
produced a potentiation of the glutamate-evoked bursts in spiking. As pointed out in the study
of dorsal horn neurons by Millar and Armstrong-James (1982), spikes evoked by glutamate
iontophoresis can be recorded along the dendritic tree of a neuron at large distances from the
soma and, in fact, there are hot spots for such glutamate-evoked activity. We have observed a
similar finding in vivo and, indeed, we believe that the glutamate-evoked activity that we
have recorded was frequently obtained at a distance of tens, if not hundreds, of microns from
the soma as we are able to track these spikes and their potential waveform over considerable
distances in vivo. Therefore, the actions of D1 receptor stimulation we have seen may be
affecting glutamatergic inputs at locations high up and above the apical dendrite of the
neuron, if not in the distal dendrites themselves. This means that we may well have detected a
functional corollary of D1-mediated blockade of calcium ion channels, presumably N- and P-
type, in vivo. Note that (1) any presynaptic influence of the D1 agonist on endogenous
glutamate release would be completely overwhelmed by the postsynaptic action of the
exogenous glutamate, and (2) we do not expect that the D1 agonist would increase
GABAergic inputs sufficiently to attenuate glutamate-evoked firing, since preliminary data
using the specific GABAA antagonist, SR9553, does not show reversal of the D1 effect.
Moreover, D1 agonists usually have to be applied, continuously, and close to fast-spiking
cells in order to affect their activity (usually as an increase in spiking). As quantified by
Krimer, Jakab, and Goldman-Rakic (1997), there are multiple appositions of tyrosine
hydroxylase-containing nerve terminals on the apical and distal dendrites of pyramidal cells
in PFC, and thus, there is a clear potential for dopamine to exert modulation of high threshold
calcium conductances at this level in the neuron (Seamans et al., 1997 and Young and Yang,
2004).
Fig. 4. D1 modulation of pyramidal cell activity evoked by exogenous glutamate. Given the
presynaptic modulation of glutamatergic transmission by D1 receptor signaling, it can be
postulated that the response of a cell to exogenous glutamate application is a direct result of
postsynaptic activation. Thus, we applied glutamate (10 mM, pH 8.0, 40–50 nA) in order to
examine D1 modulation of glutamate-evoked activity at the postsynaptic level. (a) Spike
trace of mean firing rate of a pyramidal cell recorded over a period of over 20 min. Regular
bursts of activity were evoked via cyclic application of brief pulses of glutamate (which avoid
any saturation or depolarization block). Interleaved application of the D1 agonist A77636 (in
15 s periods finishing 1s before each glutamate pulse) led to a dramatic reduction in the
evoked burst after a delay of more than 2 min. This suppression of evoked response showed
signs of only a very slow recovery. (b) Glutamate-evoked bursts in another pyramidal cell.
Application of the D1 antagonist SCH39166 led to a gradual increase in the burst amplitude
after a delay of minutes. Evoked activity was still discernibly high at the beginning of the
recovery period but showed some signs of reduction within 10 min. Subsequent application
of A77636 resulted in a gradual reduction of burst amplitude. These data suggest that there is
an endogenous dopaminergic tone that modulates the postsynaptic response to glutamate
through D1 receptor activation but activity can become even further suppressed by elevations
in D1 receptor stimulation.
Another critical part of prefrontal circuitry that is modulated by the D1 receptor and has an
important potential for interaction with the NMDA receptor is found in the local circuit
interneurons themselves. It has been shown that D1 stimulation potentiates local feed forward
excitatory inputs on to a subpopulation of fast-spiking GABAergic interneurons (Gorelova,
Seamans, & Yang, 2002). In this study, dopamine was found to induce membrane
depolarization and increase excitability in rat prefrontal cortical neurons in vitro. This
depolarization could be mimicked by a D1 agonist and one mechanism that was shown to
partly account for this effect was a D1-mediated suppression of a voltage-independent
potassium current. In slices from primate PFC, dopamine, via the D1 receptor, can increase
the excitability of fast-spiking interneurons, but not other populations of interneurons that
show adaptation in their firing (Kroner, Krimer, Lewis, & Barrionuevo, 2006). In addition,
Gao and Goldman-Rakic (2003a) demonstrated that dopamine, acting on D1 receptors, could
directly enhance the excitability of a subgroup of fast-spiking cells, such that a single EPSP
could induce spiking at a precise latency. From these findings, it is evident that D1 receptor
facilitation of feedforward excitation of fast-spiking interneurons within local circuits can
provide an important mechanism for temporally precise high frequency inhibitory inputs to
pyramidal cells within the circuit. Evidence for the functional significance of this D1 effect
was found by Gonzalez-Islas and Hablitz (2001) who demonstrated that D1 receptor
stimulation could result in a large increase in IPSCs, not only in pyramidal cells but also in
interneurons in cortical slices. These findings are also consistent with the finding that
stimulation of the VTA by local injection of NMDA produces an increase in firing in this
type of neuron in PFC (Tseng et al., 2006). It has long been considered that the activity of
parvalbumin-containing fast-spiking interneurons in neocortex is highly dependent upon
NMDA receptor-mediated glutamatergic inputs. One of the first demonstrations of this
NMDA-dependency was obtained from intracellular recordings of entorhinal cortex in vitro
which revealed that the enduring excitation of these cells by synaptic activation was
predominantly NMDA receptor-dependent (Jones & Buhl, 1993). Kawaguchi (1993) found
similar evidence for the NMDA-dependency of interneurons in PFC and further demonstrated
that the conjunction of local stimulation with induced depolarization could produce repetitive
firing in fast-spiking interneurons that was blocked by an NMDA receptor antagonist. It
should be noted, however, that in direct paired cell recordings, unitary EPSPs and EPSCs
evoked by action potentials in the presynaptic pyramidal cell, were found to be primarily
AMPA-receptor mediated in fast-spiking neurons of the rat neocortex in vitro (Angulo,
Rossier, & Audinat, 1999). Although it was found that depolarization of the postsynaptic cell
increased the NMDA component of EPSCs, the combined effects of repetitive stimulation
and depolarization were not tested. From the evidence above, it can be seen that dopamine
modulates the activity and signal processing of both pyramidal cells and fast-spiking neurons
in PFC. As we will discuss below, the perisomatic inhibition provided by the fast-spiking
neurons, primarily of the basket cell phenotype, is a critical regulator of firing and persistent
activity in the pyramidal cells and may represent an important site of dysfunction in
schizophrenia.
Both dopamine neuronal activity and NMDA-dependent changes in the state of neuronal
excitability have been implicated in learning processes and the synaptic plasticity that
underlies them. The relevance of the ―reward-related‖ activity of dopamine neurons to
learning has been a subject of intense scrutiny by Schultz and colleagues. In one of their first
predictive models (Guigon, Dorizzi, Burnod, & Schultz, 1995), they posited that dopamine
neuron firing contributed to activity-dependent changes in synaptic transmission that enabled
the development of long-term memory for recruitment of working memory processes. A
critical part of this learning arose from the ability of reward contingency to enable sustained
activity in prefrontal neurons. Hence, we are able to see the relevance of the reward
contingency studies by Watanabe (1996) and others to the adaptive nature of prefrontal
function. An essential component of this influence of reward contingency arises from the
reward prediction error encoded by dopaminergic neurons (Hollerman & Schultz, 1998).
These cells fire when reward is received unexpectedly, either at random, or at the very outset
of learning a new task. As learning proceeds, and rewards become more predictable in
parallel with increased frequency of correct responses, so the response of dopaminergic
neurons to the actual reward dwindles. At the same time, the original cue stimulus which
guides the response of the animal, now increasingly predicts reinforcement and recruits
dopamine neuron firing as a result. Moreover, in accord with learning theory, the response of
dopamine neurons and the learning of behavioral responses to conditioned stimuli were
shown to be dependent on the presence of reward prediction errors and not on the simple
association between stimulus and reward (Waelti, Dickinson, & Schultz, 2001). Thus, the
occurrence of errors in relation to an emitted behavior elicits a critical dopamine signal
during the learning process. These aspects of dopamine signaling may have important
conjunctions with those of NMDA receptor signaling during learning. Any given stimulus, in
the right context (as guided by long-term memory), may have a considerable transient
influence over neuronal activity in the forebrain. Thus, for example, simple spatial stimuli
and complex objects can evoke a seemingly sensory response in DLPFC and the inferior
convexity in nonhuman primates (Suzuki and Azuma, 1983 and Wilson et al., 1993). These
sensory responses could be phasic and/or tonic in nature and occurred while the animals
performed simple eye fixation tasks. Hence, conditions are ideal within PFC for transitions in
state that may convert this sensory information into a mnemonic representation. In other
words, it is reasonable to expect that such sensory responses are capable of producing
depolarizations in prefrontal neurons sufficient to facilitate NMDA receptor transmission.
Assuming that this state, at least partially, remains when dopamine neurons fire in relation to
an unexpected reward, then a conjunction between this state of prefrontal neurons and their
phasic dopaminergic input has the potential to modify synaptic transmission related to the
stimulus over a number of consecutive presentations. This would suggest that there is a
dopaminergic influence on NMDA-mediated synaptic plasticity, attributable to D1 receptor
signaling. In fact, there is direct evidence for this specificity of action on layer V pyramidal
cells in PFC (Young & Yang, 2005). It has been demonstrated that stimulated release of
dopamine, evoked by brief tetanic stimulation, acts via D1 receptors to promote short-term
potentiation of relatively low frequency synaptic inputs from layer V, and to suppress post-
tetanic potentiation of relatively high frequency synaptic inputs from layer III, presumably
via presynaptic inhibition of glutamate release. Moreover, the NMDA receptor-dependent
LTP produced in PFC by high frequency tetanic stimulation of the hippocampus has been
shown to require concomitant stimulation of D1 receptors in association with the stimulated
release of dopamine (Gurden, Takita, & Jay, 2000). From the evidence reviewed above, the
postsynaptic calcium-dependent facilitation of NMDA receptor currents by D1 stimulation,
combined with (i) the NMDA-mediated trapping of D1 receptors and depolarization-
dependent translocation to the synapse, and (ii) recruitment of AMPA receptors to the
membrane by a D1/NMDA receptor interaction, represents one of the most powerful
mechanisms for synaptic plasticity in the central nervous system. When this mechanism is
coupled to conditional dopamine neuron firing it may provide a fundamental neuroadaptive
substrate for learning and memory, as may have already been detected for the appetitive
instrumental learning that is dependent on the potentiation of basolateral amygdala-evoked
firing of n. accumbens neurons by D1 and NMDA receptors (Floresco et al., 2001 and Smith-
Roe and Kelley, 2000).
Finally, it must be noted that MK-801 itself is capable of producing behavioral sensitization
which can only be partially blocked by pretreatment with SCH23390 but which does lead to a
more rapid rise of dopamine levels in nucleus accumbens and D1 supersensitivity on neurons
in that region (Wolf et al., 1993). It can be posited therefore, that behavioral sensitization
results from protracted periods of elevated dopaminergic and glutamatergic transmission in
VTA and nucleus accumbens that involves prefrontal afferents to the VTA, D1 and NMDA
receptor activation, and supersensitivity of AMPA receptors in that region. Thus, the capacity
of D1/NMDA interactions to recruit AMPA receptors to the membrane and potentiate
depolarized states and persistent firing may be an essential component of neuroadaptive
mechanism in the CNS, providing a powerful engine for learning and memory but also
conferring the vulnerability that such a process can lead to disruption of prefrontal function in
behavioral adaption and its dopaminergic regulation. It should be noted that a signaling
pathway has now been described which pinpoints the significance of this interaction for
extracellular signal-regulated kinase (ERK) 1/2, an important regulator of gene expression
and cellular mechanisms of plasticity. Both acute and sensitizing administration regimes of
the partial D1 agonist SKF38393 have been found to induce a prolonged NMDA receptor-
dependent elevation of phosphorylated ERK in layers II/III of medial PFC in rats with
neonatal 6-OHDA lesions (Papadeas, Blake, Knapp, & Breese, 2004). In addition,
phosphorylated cAMP response element-binding protein (CREB) was detectable in medial
PFC but not in other brain regions after D1 sensitization. Similarly, amphetamine has been
shown to produce phosphorylation of ERK in the striatum by a combined action at D1 and
NMDA receptors and blockade of the ERK pathway attenuates the behavioral sensitization
induced by a single administration of psychostimulants (Valjent et al., 2005). These findings
led to the suggestion that the ERK pathway acts as a detector of the coincidence between
NMDA and D1 receptor stimulation in order to produce long-term adaptation of cell function
via CREB control of gene transcription. Thus, dramatic or long term changes in signaling at
either or both of these receptors may directly impact adaptive mechanisms of the cell in order
to alter its function, or en mass, to alter the function of entire regions and networks in the
brain.
Both the D1 and NMDA receptor have been shown to have a powerful influence on
prefrontal function and working memory and their interaction particularly comes into play
when neurons become depolarized in relation to afferent stimulation. Their direct interaction
not only bolsters synaptic plasticity by recruitment of AMPA receptors but also signals the
neuron to adapt to changes in dopaminergic and glutamatergic transmission. Thus the role on
this interaction in learning may be paramount, including the temporal prediction error
encoded by dopamine neurons, the mismatch between response and potential outcomes
encoded by neurons in ACC, and the valence signals to DLPFC signifying the rewards
associated with particular events. It is not surprising then, that the persistent activity that is
the engine of prefrontal function, and the recurrent excitation and inhibition it depends upon,
is highly dependent on the appropriate conjunction of signaling through these two receptors.
This dependence is highlighted by the effects of non-NMDA antagonists, not just on working
memory itself but also on the coherent guidance of behaviors and the interpretation of events
and their relation to each other and to behavior. It is equally evident from the study of D1
agonists and antagonists, under many conditions of altered dopaminergic status, that
dopamine acts as an active filter via this receptor, regulating the signal-to-noise ratio of
prefrontal neurons in a concentration dependent manner which is tuned to cognitive demands.
Implications for changes in the signaling of both receptors in schizophrenia point to the
necessity to understand the interaction of their signaling rather than focus on a ―glutamate‖ or
―dopamine‖ hypothesis, and calls for the need to investigate further the role of sensitization
in the development of cognitive deficits as well as psychosis and negative symptoms of the
disease. We hope then that this review will encourage research that will combine measures of
function at many levels from the molecular to human cognition in order to explore the
D1/NMDA interaction in tests lasting milliseconds or years. For, just as signaling through
these receptors may trigger the recruitment of a neuron into an up-state, it may also switch
whole networks in the brain into a permanently altered state
Aalto et al., 2005 S. Aalto, J. Ihalainen, J. Hirvonen, J. Kajander, H. Scheinin and H. Tanila
et al., Cortical glutamate–dopamine interaction and ketamine-induced psychotic symptoms in
man, Psychopharmacology (Berl) 182 (2005) (3), pp. 375–383 Epub 2005 Oct 19.. Full Text
via CrossRef | View Record in Scopus | Cited By in Scopus (22)
Abi-Dargham et al., 2002 A. Abi-Dargham, I.O. Mawlaw, I. Lombardo, R. Gil, D. Martinez
and Y. Huang et al., Prefrontal dopamine D1 receptors and working memory in
schizophrenia, Journal of Neuroscience 22 (2002) (9), pp. 3708–3719. View Record in
Scopus | Cited By in Scopus (242)
Adler et al., 1998 C.M. Adler, T.E. Goldberg, A.K. Malhotra, D. Pickar and A. Breier,
Effects of ketamine on thought disorder, working memory, and semantic memory in healthy
volunteers, Biological Psychiatry 43 (1998) (11), pp. 811–816. Article | PDF (175 K) | View
Record in Scopus | Cited By in Scopus (101)
Alain et al., 2002 C. Alain, H.E. McNeely, Y. He, B.K. Christensen and R. West,
Neurophysiological evidence of error-monitoring deficits in patients with schizophrenia,
Cerebral Cortex 12 (2002) (8), pp. 840–846. Full Text via CrossRef | View Record in
Scopus | Cited By in Scopus (70)
Anand et al., 2000 A. Anand, D.S. Charney, D.A. Oren, R.M. Berman, X.S. Hu and A.
Cappiello et al., Attenuation of the neuropsychiatric effects of ketamine with lamotrigine:
support for hyperglutamatergic effects of N-methyl-d-aspartate receptor antagonists, Archives
of General Psychiatry 57 (2000) (3), pp. 270–276. Full Text via CrossRef | View Record in
Scopus | Cited By in Scopus (172)
Angulo et al., 1999 M.C. Angulo, J. Rossier and E. Audinat, Postsynaptic glutamate receptors
and integrative properties of fast-spiking interneurons in the rat neocortex, Journal of
Neurophysiology 82 (1999) (3), pp. 1295–1302. View Record in Scopus | Cited By in Scopus
(39)
Arnold, 2000 S.E. Arnold, Cellular and molecular neuropathology of the parahippocampal
region in schizophrenia, Annals of the New York Academy of Sciences 911 (2000), pp. 275–
292. View Record in Scopus | Cited By in Scopus (51)
Arnsten et al., 1994 A.F.T. Arnsten, J.X. Cai, B.L. Murphy and P.S. Goldman-Rakic,
Dopamine D1 receptor mechanisms in the cognitive performance of young adult and aged
monkeys, Psychopharmacology 116 (1994), pp. 143–151. Full Text via CrossRef | View
Record in Scopus | Cited By in Scopus (251)
Arnsten and Goldman-Rakic, 1998 A.F. Arnsten and P.S. Goldman-Rakic, Noise stress
impairs prefrontal cortical cognitive function in monkeys: evidence for a hyperdopaminergic
mechanism, Archives of General Psychiatry 55 (1998) (4), pp. 362–368. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (217)
Baddeley, 1992 A. Baddeley, Working memory, Science 255 (1992) (5044), pp. 556–559.
View Record in Scopus | Cited By in Scopus (1208)
Baddeley, 1996 A. Baddeley, The fractionation of working memory, Proceedings of the
National Academy of Sciences USA 93 (1996) (24), pp. 13468–13472. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (219)
Baddeley and Hitch, 1974 A.D. Baddeley and G.J. Hitch, Working memory. In: G.A. Bower,
Editor, Recent advances in learning and motivation Vol. 8, Academic Press, New York
(1974), pp. 47–90.
Bannon and Whitty, 1997 M.J. Bannon and C.J. Whitty, Age-related and regional differences
in dopamine transporter RNA expression in human midbrain, Neurology 48 (1997), pp. 969–
977. View Record in Scopus | Cited By in Scopus (60)
Baron and Wenger, 2001 S.P. Baron and G.R. Wenger, Effects of drugs of abuse on response
accuracy and bias under a delayed matching-to-sample procedure in squirrel monkeys,
Behavioral Pharmacolology 12 (2001) (4), pp. 247–256. View Record in Scopus | Cited By
in Scopus (6)
Bartus et al., 1978a R.T. Bartus, D. Gleming and H.R. Johnson, Aging in the rhesus monkey.
Debilitating effects on short-term memory, Journal of Gerontology 33 (1978), pp. 858–871.
View Record in Scopus | Cited By in Scopus (0)
Bachevalier et al., 1991 J. Bachevalier, L.S. Landis, L.C. Walker, M. Brickson, M. Mishkin
and D.L. Price et al., Aged monkeys exhibit behavioral deficits indicative of widespread
cerebral dysfunction, Neurobiology of Aging 12 (1991), pp. 99–111. Abstract | PDF (1212 K)
| View Record in Scopus | Cited By in Scopus (110)
Bachman and Farde, 2001 L. Bachman and L. Farde, Dopamine and cognitive functioning:
brain imaging findings in Huntington‘s disease and normal aging, Scandanavian Journal of
Psychology 42 (2001), pp. 287–296.
Bartus and Johnson, 1976 R.T. Bartus and H.R. Johnson, Short-term memory in the rhesus
monkey: disruption from the anti-cholinergic scopolamine, Pharmacology, Biochemistry, and
Behavior 5 (1976) (1), pp. 39–46. Abstract | PDF (1118 K) | View Record in Scopus | Cited
By in Scopus (86)
Bartus et al., 1978b R.T. Bartus, D. Gleming and H.R. Johnson, Aging in the rhesus monkey.
Debilitating effects on short-term memory, Journal of Gerontology 33 (1978), pp. 858–871.
View Record in Scopus | Cited By in Scopus (67)
Bauer and Fuster, 1976 R.H. Bauer and J.M. Fuster, Delayed-matching and delayed-response
deficit from cooling dorsolateral prefrontal cortex in monkeys, Journal of Comparative
Physiological Psychology 90 (1976) (3), pp. 293–302. Full Text via CrossRef | View Record
in Scopus | Cited By in Scopus (77)
Beaver et al., 2006 J.D. Beaver, A.D. Lawrence, J. van Ditzhuijzen, M.H. Davis, A. Woods
and A.J. Calder, Individual differences in reward drive predict neural responses to images of
food, Journal of Neuroscience 26 (2006) (19), pp. 5160–5166. Full Text via CrossRef | View
Record in Scopus | Cited By in Scopus (71)
Bertolino et al., 2006 A. Bertolino, G. Blasi, V. Latorre, V. Rubino, A. Rampino and L.
Sinibaldi et al., Additive effects of genetic variation in dopamine regulating genes on
working memory cortical activity in human brain, Journal of Neuroscience 26 (2006) (15),
pp. 3918–3922. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (56)
Black et al., 2004 J.E. Black, I.M. Kodish, A.W. Grossman, A.Y. Klintsova, D. Orlovskaya
and V. Vostrikov et al., Pathology of layer V pyramidal neurons in the prefrontal cortex of
patients with schizophrenia, Am. J. Psychiatry 161 (2004), pp. 742–744. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (47)
Blank et al., 1997 T. Blank, I. Nijholt, U. Teichert, H. Kugler, H. Behrsing and A. Fienberg et
al., The phosphoprotein DARPP-32 mediates cAMP-dependent potentiation of striatal N-
methyl-d-aspartate responses, Proceedings of the National Academy of Sciences USA 94
(1997) (26), pp. 14859–14864. Full Text via CrossRef | View Record in Scopus | Cited By in
Scopus (79)
Broadbelt et al., 2002 K. Broadbelt, W. Byne and L.B. Jones, Evidence for a decrease in
basilar dendrites of pyramidal cells in schizophrenic medial prefrontal cortex, Schizophrenia
Research 58 (2002), pp. 75–81. Article | PDF (194 K) | View Record in Scopus | Cited By in
Scopus (54)
Brozoski et al., 1979 T.J. Brozoski, R.M. Brown, H.E. Rosvold and P.S. Goldman, Cognitive
deficit caused by regional depletion of dopamine in prefrontal cortex of rhesus monkey,
Science 205 (1979) (4409), pp. 929–932. View Record in Scopus | Cited By in Scopus (557)
Bruce and Goldberg, 1985 C.J. Bruce and M.E. Goldberg, Primate frontal eye fields. I. Single
neurons discharging before saccades, Journal of Neurophysiology 53 (1985) (3), pp. 603–
635. View Record in Scopus | Cited By in Scopus (468)
Buckner et al., 1996 R.L. Buckner, M.E. Raichle, F.M. Miezin and S.E. Petersen, Functional
anatomic studies of memory retrieval for auditory words and visual pictures, Journal of
Neuroscience 16 (1996) (19), pp. 6219–6235. View Record in Scopus | Cited By in Scopus
(219)
Buffalo et al., 1994 E.A. Buffalo, M.P. Gillam, R.R. Allen and M.G. Paule, Acute behavioral
effects of MK-801 in rhesus monkeys: assessment using an operant test battery,
Pharmacology Biochemistry and Behavior 48 (1994) (4), pp. 935–940. Abstract | PDF (606
K) | View Record in Scopus | Cited By in Scopus (31)
Butters et al., 1971 N. Butters, D. Pandya, K. Sanders and P. Dye, Behavioral deficits in
monkeys after selective lesions within the middle third of sulcus principalis, Journal of
Comparative Physiological Psychology 72 (1971), pp. 132–144.
Cai and Arnsten, 1997 J.X. Cai and A.F.T. Arnsten, Dose-dependent effects of the dopamine
D1 receptor agonists A77636 or SKF81297 on spatial working memory in aged monkeys,
Journal of Pharmacology and Experimental Therapeutics 283 (1997), pp. 183–189. View
Record in Scopus | Cited By in Scopus (99)
Carter et al., 1999 C.S. Carter, M.M. Botvinick and J.D. Cohen, The contribution of the
anterior cingulate cortex to executive processes in cognition, Reviews in the Neurosciences
10 (1999) (1), pp. 49–57. View Record in Scopus | Cited By in Scopus (230)
Castner and Goldman-Rakic, 1999 S.A. Castner and P.S. Goldman-Rakic, Long-lasting
psychotomimetic consequences of repeated low dose amphetamine exposure in rhesus
monkeys, Neuropsychopharmacology 20 (1999) (1), pp. 10–28. Article | PDF (1636 K) | Full
Text via CrossRef | View Record in Scopus | Cited By in Scopus (71)
Castner et al., 2000a S.A. Castner, G.V. Williams and P.S. Goldman-Rakic, Reversal of
antipsychotic-induced working memory deficits by short-term dopamine D1 receptor
stimulation, Science 287 (2000) (5460), pp. 2020–2022. Full Text via CrossRef | View
Record in Scopus | Cited By in Scopus (193)
Castner et al., 2000b S.A. Castner, M. Al-tikriti, R.M. Baldwin, J.P. Seibyl, R.B. Innis and
P.S. Goldman-Rakic, Behavioral changes and [123I]-IBZM equilibrium measurement of
AMPH-induced dopamine release in rhesus monkeys, Neuropsychopharmacology 22 (2000)
(1), pp. 4–13. Article | PDF (286 K) | Full Text via CrossRef | View Record in Scopus |
Cited By in Scopus (24)
Castner and Goldman-Rakic, 2003 S.A. Castner and P.S. Goldman-Rakic, Amphetamine
sensitization of hallucinatory-like behaviors is dependent on prefrontal cortex in nonhuman
primates, Biological Psychiatry 54 (2003), pp. 105–110. Article | PDF (162 K) | View
Record in Scopus | Cited By in Scopus (25)
Castner and Goldman-Rakic, 2004 S.A. Castner and P.S. Goldman-Rakic, Enhancement of
working memory in aged monkeys by a sensitizing regimen of dopamine D1 receptor
stimulation, Journal of Neuroscience 24 (2004) (6), pp. 1446–1450. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (53)
Castner et al., 2005 S.A. Castner, P.S. Vosler and P.S. Goldman-Rakic, Amphetamine
sensitization impairs cognition and reduces dopamine turnover in primate prefrontal cortex,
Biological Psychiatry 57 (2005) (7), pp. 743–751. Article | PDF (456 K) | View Record in
Scopus | Cited By in Scopus (30)
Cavada and Goldman-Rakic, 1989 C. Cavada and P.S. Goldman-Rakic, Posterior parietal
cortex in rhesus monkey: II. Evidence for segregated corticocortical networks linking sensory
and limbic areas with the frontal lobe, Journal of Comparative Neurology 287 (1989) (4), pp.
422–445. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (396)
Cavada et al., 2000 C. Cavada, T. Company, J. Tejedor, R.J. Cruz-Rizzolo and F. Reinoso-
Suarez, The anatomical connections of the macaque monkey orbitofrontal cortex, Cerebral
Cortex 10 (2000) (3), pp. 220–242. Full Text via CrossRef | View Record in Scopus | Cited
By in Scopus (218)
Cepeda et al., 1993 C. Cepeda, N.A. Buchwald and M.S. Levine, Neuromodulatory actions of
dopamine in the neostriatum are dependent upon the excitatory amino acid receptor subtypes
activated, Proceedings of the National Academy of Sciences USA 90 (1993) (20), pp. 9576–
9580. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (292)
Cepeda and Levine, 2006 Cepeda, C., Levine, M.S. (2006). Where do you think you are
going? The NMDA-D1 receptor trap. Science STKE, (333), pe20.
Cepeda et al., 1999 C. Cepeda, Z. Li, H.C. Cromwell, K.L. Altemus, C.A. Crawford and E.A.
Nansen et al., Electrophysiological and morphological analyses of cortical neurons obtained
from children with catastrophic epilepsy: dopamine receptor modulation of glutamatergic
responses, Developmental Neuroscience 21 (1999) (3-5), pp. 223–235. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (29)
Chafee and Goldman-Rakic, 1998 M.V. Chafee and P.S. Goldman-Rakic, Matching patterns
of activity in primate prefrontal area 8a and parietal area 7ip neurons during a spatial working
memory task, Journal of Neurophysiology 79 (1998) (6), pp. 2919–2940. View Record in
Scopus | Cited By in Scopus (276)
Chambers et al., 1996 R.A. Chambers, J. Moore, J.P. McEvoy and E.D. Levin, Cognitive
effects of neonatal hippocampal lesions in a rat model of schizophrenia,
Neuropsychopharmacology 15 (1996) (6), pp. 587–594. Full Text via CrossRef | View
Record in Scopus | Cited By in Scopus (97)
Chen et al., 2004 G. Chen, P. Greengard and Z. Yan, Potentiation of NMDA receptor currents
by dopamine D1 receptors in prefrontal cortex, Proceedings of the National Academy of
Sciences 101 (2004) (8), pp. 2596–25600.
Chiodo and Berger, 1986 L.A. Chiodo and T.W. Berger, Interactions between dopamine and
amino acid-induced excitation and inhibition in the striatum, Brain Research 375 (1986) (1),
pp. 198–203. Abstract | PDF (515 K) | View Record in Scopus | Cited By in Scopus (62)
Cohen et al., 1997 J.D. Cohen, W.M. Perlstein, T.S. Braver, L.E. Nystrom, D.C. Noll and J.
Jonides et al., Temporal dynamics of brain activation during a working memory task, Nature
386 (1997) (6625), pp. 604–608. Full Text via CrossRef
Collins et al., 1998 P. Collins, A.C. Roberts, R. Dias, B.J. Everitt and T.W. Robbins,
Perseveration and strategy in a novel spatial self-ordered sequencing task for nonhuman
primates: effects of excitotoxic lesions and dopamine depletions of the prefrontal cortex,
Journal of Cognitive Neuroscience 10 (1998) (3), pp. 332–354. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (91)
Condy et al., 2005 C. Condy, N. Wattiez, S. Rivaud-Pechoux and B. Gaymard, Ketamine-
induced distractibility: an oculomotor study in monkeys, Biological Psychiatry 57 (2005) (4),
pp. 366–372. Article | PDF (283 K) | View Record in Scopus | Cited By in Scopus (9)
Constantinidis et al., 2001 C. Constantinidis, M.N. Franowicz and P.S. Goldman-Rakic, The
sensory nature of mnemonic representation in the primate prefrontal cortex, Nature
Neuroscience 4 (2001) (3), pp. 311–316. Full Text via CrossRef | View Record in Scopus |
Cited By in Scopus (81)
Constantinidis et al., 2002 C. Constantinidis, G.V. Williams and P.S. Goldman-Rakic, A role
for inhibition in shaping the temporal flow of information in the prefrontal cortex, Nature
Neuroscience 5 (2002) (2), pp. 175–180. Full Text via CrossRef | View Record in Scopus |
Cited By in Scopus (136)
Cools et al., 2002 R. Cools, E. Stefanova, R.A. Barker, T.W. Robbins and A.M. Owen,
Dopaminergic modulation of high-level cognition in Parkinson‘s disease: the role of the
prefrontal cortex revealed by PET, Brain 125 (2002), pp. 584–594. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (138)
Coyle, 2006 J.T. Coyle, Glutamate and Schizophrenia: beyond the dopamine hypothesis,
Cellular and Molecular Neurobiology (2006) [Epub ahead of print]..
Criswell et al., 1989 H. Criswell, R.A. Mueller and G.R. Breese, Priming of D1-dopamine
receptor responses: long-lasting behavioral supersensitivity to a D1-dopamine agonist
following repeated administration to neonatal 6-OHDA-lesioned rats, Journal of
Neuroscience 9 (1989) (1), pp. 125–133. View Record in Scopus | Cited By in Scopus (49)
Criswell et al., 1990 H.E. Criswell, R.A. Mueller and G.R. Breese, Long-term D1-dopamine
receptor sensitization in neonatal 6-OHDA-lesioned rats is blocked by an NMDA antagonist,
Brain Research 512 (1990) (2), pp. 284–290. Abstract | PDF (711 K) | View Record in
Scopus | Cited By in Scopus (30)
Daniel et al., 1991 D.G. Daniel, D.R. Weinberger, D.W. Jones, J.R. Zigun, R. Coppola and S.
Handel et al., The effect of amphetamine on regional cerebral blood flow during cognitive
activation in schizophrenia, Journal of Neuroscience 11 (1991) (7), pp. 1907–1917. View
Record in Scopus | Cited By in Scopus (161)
de Keyser et al., 1990 J. de Keyser, J.P. de Backer, G. Vauquelin and G. Ebinger, The effect
of aging on the D1 dopamine receptors in human frontal cortex, Brain Research 528 (1990),
pp. 308–310. Abstract | PDF (242 K) | View Record in Scopus | Cited By in Scopus (38)
Dias et al., 1996 R. Dias, T.W. Robbins and A.C. Roberts, Dissociation in prefrontal cortex
of affective and attentional shifts, Nature 380 (1996) (6569), pp. 69–72. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (630)
Durstewitz et al., 2000a D. Durstewitz, J.K. Seamans and T.J. Sejnowski,
Neurocomputational models of working memory, Nature Neuroscience 3 (2000) (Suppl), pp.
1184–1191. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (195)
Durstewitz et al., 2000b D. Durstewitz, J.K. Seamans and T.J. Sejnowski, Dopamine-
mediated stabilization of delay-period activity in a network model of prefrontal cortex,
Journal of Neurophysiology 83 (2000) (3), pp. 1733–1750. View Record in Scopus | Cited By
in Scopus (202)
Durstewitz and Seamans, 2002 D. Durstewitz and J.K. Seamans, The computational role of
dopamine D1 receptors in working memory, Neural Networks 15 (2002) (4-6), pp. 561–572.
Article | PDF (1073 K) | View Record in Scopus | Cited By in Scopus (92)
Egan et al., 2001 M.F. Egan, T.E. Goldberg, B.S. Kolachana, J.H. Callicott, C.M. Mazzanti
and R.E. Straub et al., Effect of COMT Val 108/158 Met genotype on frontal lobe function
and risk for schizophrenia, Proceedings of the National Academy of Sciences USA 98 (2001)
(12), pp. 6917–6922. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus
(1019)
Ellinwood et al., 1973 E.H. Ellinwood Jr., A. Sudilovsky and L.M. Nelson, Evolving
behavior in the clinical and experimental amphetamine (model) psychosis, Am. J. Psychiatry
130 (1973) (10), pp. 1088–1093. View Record in Scopus | Cited By in Scopus (85)
Fernandez-Ruiz et al., 1995 J. Fernandez-Ruiz, D.J. Doudet and T.G. Aigner, Long-term
cognitive impairment in MPTP-treated rhesus monkeys, Neuroreport 7 (1995) (1), pp. 102–
104. View Record in Scopus | Cited By in Scopus (19)
Fernandez-Ruiz et al., 1999 J. Fernandez-Ruiz, D. Doudet and T.G. Aigner, Spatial memory
improvement by levodopa in parkinsonian MPTP-treated monkeys, Psychopharmacology
(Berl) 147 (1999) (1), pp. 104–107. View Record in Scopus | Cited By in Scopus (13)
Flemenbaum, 1977 A. Flemenbaum, Dopamine receptors hypersensitivity: further
confirmation following drug abuse model, Advances in Experimental Medicine and Biology
90 (1977), pp. 207–217. View Record in Scopus | Cited By in Scopus (1)
Floresco et al., 2001 S.B. Floresco, C.D. Blaha, C.R. Yang and A.G. Phillips, Dopamine D1
and NMDA receptors mediate potentiation of basolateral amygdala-evoked firing of nucleus
accumbens neurons, Journal of Neuroscience 21 (2001) (16), pp. 6370–6376. View Record in
Scopus | Cited By in Scopus (50)
Flores-Hernandez et al., 2002 J. Flores-Hernandez, C. Cepeda, E. Hernandez-Echeagaray,
C.R. Calvert, E.S. Jokel and A.A. Fienberg et al., Dopamine enhancement of NMDA currents
in dissociated medium-sized striatal neurons: role of D1 receptors and DARPP-32, Journal of
Neurophysiology 88 (2002) (6), pp. 3010–3020. Full Text via CrossRef | View Record in
Scopus | Cited By in Scopus (106)
Frederick et al., 1995 D.L. Frederick, M.P. Gillam, R.R. Allen and M.G. Paule, Acute
behavioral effects of phencyclidine on rhesus monkey performance in an operant test battery,
Pharmacology, Biochemistry, and Behavior 52 (1995) (4), pp. 789–797. Article | PDF (1064
K) | View Record in Scopus | Cited By in Scopus (22)
Funahashi et al., 1989 S. Funahashi, C.J. Bruce and P.S. Goldman-Rakic, Mnemonic coding
of visual space in the monkey‘s dorsolateral prefrontal cortex, Journal of Neurophysiology 61
(1989) (2), pp. 331–349. View Record in Scopus | Cited By in Scopus (841)
Funahashi et al., 1990 S. Funahashi, C.J. Bruce and P.S. Goldman-Rakic, Visuospatial coding
in primate prefrontal neurons revealed by oculomotor paradigms, Journal of Neurophysiology
63 (1990) (4), pp. 814–831. View Record in Scopus | Cited By in Scopus (209)
Funahashi et al., 1991 S. Funahashi, C.J. Bruce and P.S. Goldman-Rakic, Neuronal activity
related to saccadic eye movements in the monkey‘s dorsolateral prefrontal cortex, Journal of
Neurophysiology 65 (1991) (6), pp. 1464–1483. View Record in Scopus | Cited By in Scopus
(141)
Funahashi et al., 1993 S. Funahashi, C.J. Bruce and P.S. Goldman-Rakic, Dorsolateral
prefrontal lesions and oculomotor delayed-response performance: evidence for mnemonic
―scotomas‖, Journal of Neuroscience 13 (1993) (4), pp. 1479–1497. View Record in Scopus |
Cited By in Scopus (251)
Fuster, 1997 J.M. Fuster, The Prefrontal Cortex, Raven Press, New York (1997).
Fuster and Alexander, 1971 J.M. Fuster and G.E. Alexander, Neuron activity related to short-
term memory, Science 173 (1971), pp. 652–654. View Record in Scopus | Cited By in Scopus
(413)
Fuster et al., 1985 J.M. Fuster, R.H. Bauer and J.P. Jervey, Functional interactions between
inferotemporal and prefrontal cortex in a cognitive task, Brain Research 330 (1985) (2), pp.
299–307. Abstract | PDF (652 K) | View Record in Scopus | Cited By in Scopus (154)
Gao et al., 2001 W-J. Gao, L.S. Krimer and P.S. Goldman-Rakic, Presynaptic regulation of
recurrent excitation by D1 receptors in prefrontal circuits, Proceedings of the National
Academy of Sciences USA 98 (2001), pp. 295–300. Full Text via CrossRef | View Record in
Scopus | Cited By in Scopus (113)
Gao and Goldman-Rakic, 2003a W.J. Gao and P.S. Goldman-Rakic, Selective modulation of
excitatory and inhibitory microcircuits by dopamine, Proceedings of the National Academy of
Sciences USA 100 (2003) (5), pp. 2836–2841. Full Text via CrossRef | View Record in
Scopus | Cited By in Scopus (56)
Garey et al., 1998 L.J. Garey, W.Y. Ong, T.S. Patel, M. Kanani, A. Davis and A.M. Mortimer
et al., Reduced dendritic spine density on cerebral cortical pyramidal neurons in
schizophrenia, Journal of Neurology Neurosurgery Psychiatry 65 (1998), pp. 446–453. Full
Text via CrossRef | View Record in Scopus | Cited By in Scopus (210)
Gao et al., 2003b W.J. Gao, Y. Wang and P.S. Goldman-Rakic, Dopamine modulation of
perisomatic and peridendritic inhibition in prefrontal cortex, Journal of Neuroscience 23
(2003) (5), pp. 1622–1630. View Record in Scopus | Cited By in Scopus (40)
Gattass et al., 1990 R. Gattass, M.G. Rosa, A.P. Sousa, M.C. Pinon, M. Fiorani Junior and S.
Neuenschwander, Cortical streams of visual information processing in primates, Brazilian
Journal of Medical and Biological Research 23 (1990) (5), pp. 375–393. View Record in
Scopus | Cited By in Scopus (25)
Gehring and Fencsik, 2001 W.J. Gehring and D.E. Fencsik, Functions of the medial frontal
cortex in the processing of conflict and errors, Journal of Neuroscience 21 (2001) (23), pp.
9430–9437. View Record in Scopus | Cited By in Scopus (132)
Ghent et al., 1962 L. Ghent, M. Mishkin and H.L. Teuber, Short-term memory after frontal-
lobe injury in man, Journal of Comparative and Physiological Psychology 55 (1962), pp.
705–709. Abstract | Full Text via CrossRef | View Record in Scopus | Cited By in Scopus
(18)
Ghoneim et al., 1985 M.M. Ghoneim, J.V. Hinrichs, S.P. Mewaldt and R.C. Petersen,
Ketamine: behavioral effects of subanesthetic doses, Journal of Clinical
Psychopharmacology 5 (1985) (2), pp. 70–77. View Record in Scopus | Cited By in Scopus
(76)
Giorgetti et al., 2001 M. Giorgetti, G. Hotsenpiller, P. Ward, T. Teppen and E.M. Wolf,
Amphetamine-induced plasticity of AMPA receptors in the ventral tegmental area: effects on
extracellular levels of dopamine and glutamate in freely moving rats, Journal of
Neuroscience 21 (2001) (16), pp. 6362–6369. View Record in Scopus | Cited By in Scopus
(45)
Glahn et al., 2002 D.C. Glahn, J. Kim, M.S. Cohen, V.P. Poutanen, S. Therman and S. Bava
et al., Maintenance and manipulation in spatial working memory: dissociations in the
prefrontal cortex, Neuroimage 17 (2002) (1), pp. 201–213. Abstract | PDF (493 K) | View
Record in Scopus | Cited By in Scopus (47)
Glantz and Lewis, 2000 L.A. Glantz and D.A. Lewis, Decreased dendritic spine density on
prefrontal cortical pyramidal neurons in schizophrenia, Archives of General Psychiatry 57
(2000), pp. 65–73. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus
(352)
Goldberg and Bruce, 1986 M.E. Goldberg and C.J. Bruce, The role of the arcuate frontal eye
fields in the generation of saccadic eye movements, Progress in Brain Research 64 (1986),
pp. 143–154. Abstract | View Record in Scopus | Cited By in Scopus (2)
Goldberg et al., 2003 T.E. Goldberg, M.F. Egan, T. Gscheidle, R. Coppola, T. Weickert and
B.S. Kolachana et al., Executive subprocesses in working memory: relationship to catechol-
O-methyltransferase Val158Met genotype and schizophrenia, Archives of General Psychiatry
60 (2003) (9), pp. 889–896. Full Text via CrossRef | View Record in Scopus | Cited By in
Scopus (262)
Goldman-Rakic, 1987 P.S. Goldman-Rakic, Circuitry of primate prefrontal cortex and
regulation of behavior by representational memory. In: F. Plum, Editor, Handbook of
physiology, the nervous system, functions of the brain, American Physiological Society,
Bethesda (1987), pp. 373–417.
Goldman-Rakic, 1990 P.S. Goldman-Rakic, Cellular and circuit basis of working memory in
prefrontal cortex of nonhuman primates, Progress in Brain Research 85 (1990), pp. 325–335.
Goldman-Rakic, 2000 P. Goldman-Rakic, Localization of function all over again,
Neuroimage 11 (2000) (5 Pt 1), pp. 451–457. Abstract | PDF (55 K) | View Record in Scopus
| Cited By in Scopus (33)
Goldman-Rakic and Brown, 1981 P.S. Goldman-Rakic and R.M. Brown, Regional changes
in monoamines in cerebral cortex and subcortical structures of aging rhesus monkeys,
Neuroscience 6 (1981), pp. 177–187. Abstract | PDF (1205 K) | View Record in Scopus |
Cited By in Scopus (119)
Gonon, 1997 F. Gonon, Prolonged and extrasynaptic excitatory action of dopamine mediated
by D1 receptors in the rat striatum in vivo, Journal of Neuroscience 17 (1997) (15), pp.
5972–5978. View Record in Scopus | Cited By in Scopus (155)
Gonzalez-Burgos et al., 2002 G. Gonzalez-Burgos, S. Kroner, L.S. Krimer, J.K. Seamans,
N.N. Urban and D.A. Henze et al., Dopamine modulation of neuronal function in the monkey
prefrontal cortex, Physiology and Behavior 77 (2002) (4-5), pp. 537–543. Article | PDF (484
K) | View Record in Scopus | Cited By in Scopus (21)
Gonzalez-Islas and Hablitz, 2001 C. Gonzalez-Islas and J.J. Hablitz, Dopamine inhibition of
evoked IPSCs in rat prefrontal cortex, Journal of Neurophysiology 86 (2001) (6), pp. 2911–
2918. View Record in Scopus | Cited By in Scopus (34)
Gorelova and Yang, 2000 N.A. Gorelova and C.R. Yang, Dopamine D1/D5 receptor
activation modulates a persistent sodium current in rat prefrontal cortical neurons in vitro,
Journal of Neurophysiology 84 (2000) (1), pp. 75–87. View Record in Scopus | Cited By in
Scopus (79)
Gorelova et al., 2002 N. Gorelova, J.K. Seamans and C.R. Yang, Mechanisms of dopamine
activation of fast-spiking interneurons that exert inhibition in rat prefrontal cortex, Journal of
Neurophysiology 88 (2002) (6), pp. 3150–3166. Full Text via CrossRef | View Record in
Scopus | Cited By in Scopus (94)
Guigon et al., 1995 E. Guigon, B. Dorizzi, Y. Burnod and W. Schultz, Neural correlates of
learning in the prefrontal cortex of the monkey: a predictive model, Cerebral Cortex 5 (1995)
(2), pp. 135–147. View Record in Scopus | Cited By in Scopus (26)
Gurden et al., 2000 H. Gurden, M. Takita and T.M. Jay, Essential role of D1 but not D2
receptors in the NMDA receptor-dependent long-term potentiation at hippocampal-prefrontal
cortex synapses in vivo, Journal of Neuroscience 20 (2000) (22), p. RC106. View Record in
Scopus | Cited By in Scopus (142)
Guo et al., 2003 N. Guo, D.R. Hwang, E.S. Lo, Y.Y. Huang, M. Laruelle and A. Abi-
Dargham, Dopamine depletion and in vivo binding of PET D1 receptor radioligands:
implications for imaging studies in schizophrenia, Neuropsychopharmacology 28 (2003) (9),
pp. 1703–1711. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (33)
Harada et al., 2002 N. Harada, S. Nishiyama, K. Satoh, D. Fukumoto, T. Kakiuchi and H.
Tsukada, Age-related changes in the striatal dopamine system in the living brain: a
multiparametric study in conscious monkeys, Synapse 45 (2002), pp. 38–45. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (22)
Harrison, 1999 P.J. Harrison, The neuropathology of schizophrenia. A critical review of the
data and their interpretation, Brain 122 (1999) (Pt 4), pp. 593–624. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (805)
Henby and Trojanowski, 2003 S.E. Henby and J.Q. Trojanowski, Neuron-specific age-related
decreases in dopamine receptor mRNAs, Journal of Comparative Neurology 456 (2003), pp.
176–183.
Hernandez-Lopez et al., 1997 S. Hernandez-Lopez, J. Bargas, D.J. Surmeier, A. Reyes and E.
Galarraga, D1 receptor activation enhances evoked discharge in neostriatal medium spiny
neurons by modulating an L-type Ca2+ conductance, Journal of Neuroscience 17 (1997) (9),
pp. 3334–3342. View Record in Scopus | Cited By in Scopus (242)
Hertel et al., 1999 P. Hertel, M.V. Fagerquist and T.H. Svensson, Enhanced cortical
dopamine output and antipsychotic-like effects of raclopride by alpha2 adrenoceptor
blockade, Science 286 (1999) (5437), pp. 105–107. Full Text via CrossRef | View Record in
Scopus | Cited By in Scopus (110)
Hikosaka and Watanabe, 2000 K. Hikosaka and M. Watanabe, Delay activity of orbital and
lateral prefrontal neurons of the monkey varying with different rewards, Cerebral Cortex 10
(2000) (3), pp. 263–271. Full Text via CrossRef | View Record in Scopus | Cited By in
Scopus (164)
Hikosaka and Watanabe, 2004 K. Hikosaka and M. Watanabe, Long- and short-range reward
expectancy in the primate orbitofrontal cortex, European Journal of Neuroscience 19 (2004)
(4), pp. 1046–1054. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus
(22)
Holcomb et al., 1996 H.H. Holcomb, N.G. Cascella, G.K. Thaker, D.R. Medoff, R.F. Dannals
and C.A. Tamminga, Functional sites of neuroleptic drug action in the human brain:
PET/FDG studies with and without haloperidol, American Journal of Psychiatry 153 (1996)
(1), pp. 41–49. View Record in Scopus | Cited By in Scopus (153)
Holcomb et al., 2005 H.H. Holcomb, A.C. Lahti, D.R. Medoff, T. Cullen and C.A.
Tamminga, Effects of noncompetitive NMDA receptor blockade on anterior cingulate
cerebral blood flow in volunteers with schizophrenia, Neuropsychopharmacology 30 (2005)
(12), pp. 2275–2282. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus
(19)
Hollerman and Schultz, 1998 J.R. Hollerman and W. Schultz, Dopamine neurons report an
error in the temporal prediction of reward during learning, Nature Neuroscience 1 (1998) (4),
pp. 304–309. View Record in Scopus | Cited By in Scopus (215)
Holroyd and Coles, 2002 C.B. Holroyd and M.G. Coles, The neural basis of human error
processing: reinforcement learning, dopamine, and the error-related negativity, Psychology
Review 109 (2002) (4), pp. 679–709. Abstract | Full Text via CrossRef | View Record in
Scopus | Cited By in Scopus (557)
Hu and White, 1997 X.T. Hu and F.J. White, Dopamine enhances glutamate-induced
excitation of rat striatal neurons by cooperative activation of D1 and D2 class receptors,
Neuroscience Letters 224 (1997) (1), pp. 61–65. Article | PDF (156 K) | View Record in
Scopus | Cited By in Scopus (67)
Hu et al., 2002 X.T. Hu, T.E. Koeltzow, D.C. Cooper, G.S. Robertson, F.J. White and P.
Vezina, Repeated ventral tegmental area amphetamine administration alters dopamine D1
receptor signaling in the nucleus accumbens, Synapse 45 (2002) (3), pp. 159–170. Full Text
via CrossRef | View Record in Scopus | Cited By in Scopus (26)
Hu and Wang, 1988 X.T. Hu and R.Y. Wang, Comparison of effects of D-1 and D-2
dopamine receptor agonists on neurons in the rat caudate putamen: an electrophysiological
study, Journal of Neuroscience 8 (1988) (11), pp. 4340–4348. View Record in Scopus | Cited
By in Scopus (46)
Ichikawa et al., 2001 J. Ichikawa, H. Ishii, S. Bonaccorso, W.L. Fowler, I.A. O‘Laughlin and
H.Y. Meltzer, 5-HT(2A) and D(2) receptor blockade increases cortical DA release via 5-
HT(1A) receptor activation: a possible mechanism of atypical antipsychotic-induced cortical
dopamine release, Journal of Neurochemistry 76 (2001) (5), pp. 1521–1531. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (245)
Jacobsen, 1935 C.F. Jacobsen, Functions of frontal association areas in primates, Archives of
Neurology and Psychiatry 33 (1935), pp. 358–369.
Javitt and Zukin, 1991 D.C. Javitt and S.R. Zukin, Recent advances in the phencyclidine
model of schizophrenia, American Journal of Psychiatry 148 (1991) (10), pp. 1301–1308.
View Record in Scopus | Cited By in Scopus (1244)
Javitt et al., 2000 D.C. Javitt, M. Jayachandra, R.W. Lindsley, C.M. Specht and C.E.
Schroeder, Schizophrenia-like deficits in auditory P1 and N1 refractoriness induced by the
psychomimetic agent phencyclidine (PCP), Clinical Neurophysiology 111 (2000) (5), pp.
833–836. Abstract | PDF (113 K) | View Record in Scopus | Cited By in Scopus (30)
Jensen et al., 2006 J. Jensen, A.J. Smith, M. Willeit, A.P. Crawley, D.J. Mikulis and I. Vitcu
et al., Separate brain regions code for salience vs. valence during reward prediction in
humans, Human Brain Mapping (2006) [Epub ahead of print]..
Jentsch et al., 1997 J.D. Jentsch, D.E. Redmond Jr., J.D. Elsworth, J.R. Taylor, K.D.
Youngren and R.H. Roth, Enduring cognitive deficits and cortical dopamine dysfunction in
monkeys after long-term administration of phencyclidine, Science 277 (1997) (5328), pp.
953–955. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (205)
Jentsch et al., 1999a J.D. Jentsch, J.R. Taylor, J.D. Elsworth, D.E. Redmond Jr. and R.H.
Roth, Altered frontal cortical dopaminergic transmission in monkeys after subchronic
phencyclidine exposure: involvement in frontostriatal cognitive deficits, Neuroscience 90
(1999) (3), pp. 823–832. Article | PDF (212 K) | View Record in Scopus | Cited By in Scopus
(44)
Jentsch et al., 1999b J.D. Jentsch, J.R. Taylor, D.E. Redmond Jr., J.D. Elsworth, K.D.
Youngren and R.H. Roth, Dopamine D4 receptor antagonist reversal of subchronic
phencyclidine-induced object retrieval/detour deficits in monkeys, Psychopharmacology 142
(1999) (1), pp. 78–84. Full Text via CrossRef
Jentsch et al., 2000 J.D. Jentsch, R.H. Roth and J.R. Taylor, Object retrieval/detour deficits in
monkeys produced by prior subchronic phencyclidine administration: evidence for cognitive
impulsivity, Biological Psychiatry 48 (2000) (5), pp. 415–424. Article | PDF (156 K) | View
Record in Scopus | Cited By in Scopus (23)
Jones and Buhl, 1993 R.S. Jones and E.H. Buhl, Basket-like interneurones in layer II of the
entorhinal cortex exhibit a powerful NMDA-mediated synaptic excitation, Neuroscience
Letters 149 (1993) (1), pp. 35–39. Abstract | PDF (431 K) | View Record in Scopus | Cited
By in Scopus (61)
Kalivas and Stewart, 1991 P.W. Kalivas and J. Stewart, Dopamine transmission in the
initiation and expression of drug- and stress-induced sensitization of motor activity, Brain
Research. Brain Research Reviews 16 (1991) (3), pp. 223–244. Abstract | PDF (3480 K) |
View Record in Scopus | Cited By in Scopus (1160)
Kalus et al., 2000 P. Kalus, T.J. Muller, W. Zuschratter and D. Senitz, The dendritic
architecture of prefrontal pyramidal neurons in schizophrenia patients, Neuroreport 11
(2000), pp. 3621–3625. View Record in Scopus | Cited By in Scopus (44)
Karler et al., 1997 R. Karler, J.B. Bedingfield, D.K. Thai and L.D. Calder, The role of the
frontal cortex in the mouse in behavioral sensitization to amphetamine, Brain Research 757
(1997) (2), pp. 228–235. Article | PDF (180 K) | View Record in Scopus | Cited By in Scopus
(38)
Karler et al., 1989 R. Karler, L.D. Calder, I.A. Chaudhry and S.A. Turkanis, Blockade of
―reverse tolerance‖ to cocaine and amphetamine by MK-801, Life Sciences 45 (1989) (7), pp.
599–606. Abstract | View Record in Scopus | Cited By in Scopus (278)
Karler et al., 1991 R. Karler, L.D. Calder and S.A. Turkanis, DNQX blockade of
amphetamine behavioral sensitization, Brain Research 552 (1991) (2), pp. 295–300. Abstract
| PDF (553 K) | View Record in Scopus | Cited By in Scopus (117)
Kawaguchi, 1993 Y. Kawaguchi, Groupings of nonpyramidal and pyramidal cells with
specific physiological and morphological characteristics in rat frontal cortex, Journal of
Neurophysiology 69 (1993) (2), pp. 416–431. View Record in Scopus | Cited By in Scopus
(160)
Kawaguchi, 2001 Y. Kawaguchi, Distinct firing patterns of neuronal subtypes in cortical
synchronized activities, Journal of Neuroscience 21 (2001) (18), pp. 7261–7272. View
Record in Scopus | Cited By in Scopus (31)
Keith et al., 1991 V.A. Keith, R.S. Mansbach and M.A. Geyer, Failure of haloperidol to
block the effects of phencyclidine and dizocilpine on prepulse inhibition of startle, Biological
Psychiatry 30 (1991) (6), pp. 557–566. Abstract | PDF (1303 K) | View Record in Scopus |
Cited By in Scopus (132)
Kolata, 1983 G. Kolata, Monkey model of Parkinson‘s disease, Science 220 (1983) (4598), p.
705. View Record in Scopus | Cited By in Scopus (6)
Krimer et al., 1997 L.S. Krimer, R.L. Jakab and P.S. Goldman-Rakic, Quantitative three-
dimensional analysis of the catecholaminergic innervation of identified neurons in the
macaque prefrontal cortex, Journal of Neuroscience 17 (1997) (19), pp. 7450–7461. View
Record in Scopus | Cited By in Scopus (47)
Kroner et al., 2006 S. Kroner, L.S. Krimer, D.A. Lewis and G. Barrionuevo, Dopamine
increases inhibition in the monkey dorsolateral prefrontal cortex through cell type-specific
modulation of interneurons, Cerebral Cortex (2006) [Epub ahead of print]..
Krystal et al., 1994 J.H. Krystal, L.P. Karper, J.P. Seibyl, G.K. Freeman, R. Delaney and J.D.
Bremner et al., Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in
humans. Psychotomimetic, perceptual, cognitive, and neuroendocrine responses, Archives of
General Psychiatry 51 (1994) (3), pp. 199–214. View Record in Scopus | Cited By in Scopus
(896)
Krystal et al., 2005a J.H. Krystal, E.B. Perry Jr., R. Gueorguieva, A. Belger, S.H. Madonick
and A. Abi-Dargham et al., Comparative and interactive human psychopharmacologic effects
of ketamine and amphetamine: implications for glutamatergic and dopaminergic model
psychoses and cognitive function, Archives of General Psychiatry 62 (2005) (9), pp. 985–
994. Full Text via CrossRef
Krystal et al., 2005b J.H. Krystal, W. Abi-Saab, E. Perry, D.C. D‘Souza, N. Liu and R.
Gueorguieva et al., Preliminary evidence of attenuation of the disruptive effects of the
NMDA glutamate receptor antagonist, ketamine, on working memory by pretreatment with
the group II metabotropic glutamate receptor agonist, LY354740, in healthy human subjects,
Psychopharmacology (Berl) 179 (2005) (1), pp. 303–309 Epub 2004 Aug 10.. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (55)
Kubota and Niki, 1971 K. Kubota and H. Niki, Prefrontal cortical unit activity and delayed
alternation performance in monkeys, Journal of Neurophysiology 34 (1971) (3), pp. 337–347.
View Record in Scopus | Cited By in Scopus (190)
Lahti et al., 1995 A.C. Lahti, H.H. Holcomb, D.R. Medoff and C.A. Tamminga, Ketamine
activates psychosis and alters limbic blood flow in schizophrenia, Neuroreport 6 (1995) (6),
pp. 869–872. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (184)
Lange et al., 1992 K.W. Lange, T.W. Robbins, C.D. Marsden, M. James, A.M. Owen and
G.M. Paul, l-dopa withdrawal in Parkinson‘s disease selectively impairs cognitive
performance in tests sensitive to frontal lobe dysfunction, Psychopharmacology 107 (1992)
(2-3), pp. 394–404. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus
(270)
Langston et al., 1984 J.W. Langston, E.B. Langston and I. Irwin, MPTP-induced
parkinsonism in human and non-human primates—clinical and experimental aspects, Acta
Neurologica Scandinavica, Suppl 100 (1984), pp. 49–54. View Record in Scopus | Cited By
in Scopus (77)
Lavin et al., 2005 A. Lavin, L. Nogueira, C.C. Lapish, R.M. Wightman, P.E. Phillips and J.K.
Seamans, Mesocortical dopamine neurons operate in distinct temporal domains using
multimodal signaling, Journal of Neuroscience 25 (2005) (20), pp. 5013–5023. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (72)
Lee et al., 2003 K.H. Lee, L.M. Williams, M. Breakspear and E. Gordon, Synchronous
gamma activity: a review and contribution to an integrative neuroscience model of
schizophrenia, Brain Research Reviews 41 (2003) (1), pp. 57–78. Article | PDF (183 K) |
View Record in Scopus | Cited By in Scopus (134)
Leon and Shadlen, 1999 M.I. Leon and M.N. Shadlen, Effect of expected reward magnitude
on the response of neurons in the dorsolateral prefrontal cortex of the macaque, Neuron 24
(1999) (2), pp. 415–425. Article | PDF (338 K) | View Record in Scopus | Cited By in Scopus
(194)
Leung et al., 2002 H.C. Leung, J.C. Gore and P.S. Goldman-Rakic, Sustained mnemonic
response in the human middle frontal gyrus during on-line storage of spatial memoranda,
Journal of Cognitive Neuroscience 14 (2002) (4), pp. 659–671. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (111)
Levin et al., 2005 E.D. Levin, A. Petro and D.P. Caldwell, Nicotine and clozapine actions on
pre-pulse inhibition deficits caused by N-methyl-d-aspartate (NMDA) glutamatergic receptor
blockade, Progress in Neuropsychopharmacology and Biological Psychiatry 29 (2005) (4),
pp. 581–586. Article | PDF (302 K) | View Record in Scopus | Cited By in Scopus (15)
Levine et al., 1996 M.S. Levine, K.L. Altemus, C. Cepeda, H.C. Cromwell, C. Crawford and
M.A. Ariano et al., Modulatory actions of dopamine on NMDA receptor-mediated responses
are reduced in D1A-deficient mutant mice, Journal of Neuroscience 16 (1996) (18), pp.
5870–5882. View Record in Scopus | Cited By in Scopus (104)
Levy and Goldman-Rakic, 1999 R. Levy and P.S. Goldman-Rakic, Association of storage
and processing functions in the dorsolateral prefrontal cortex of the nonhuman primate,
Journal of Neuroscience 19 (1999) (12), pp. 5149–5158. View Record in Scopus | Cited By
in Scopus (82)
Levy and Goldman-Rakic, 2000 R. Levy and P.S. Goldman-Rakic, Segregation of working
memory functions within the dorsolateral prefrontal cortex, Experimental Brain Research
133 (2000) (1), pp. 23–32. Full Text via CrossRef | View Record in Scopus | Cited By in
Scopus (196)
Lewis and Gonzalez-Burgos, 2000 D.A. Lewis and G. Gonzalez-Burgos, Intrinsic excitatory
connections in the prefrontal cortex and the pathophysiology of schizophrenia, Brain
Research Bulletin 52 (2000) (5), pp. 309–317. Article | PDF (949 K) | View Record in
Scopus | Cited By in Scopus (47)
Lewis and O‘Donnell, 2000 B.L. Lewis and P. O‘Donnell, Ventral tegmental area afferents to
the prefrontal cortex maintain membrane potential ‗up‘ states in pyramidal neurons via D(1)
dopamine receptors, Cerebral Cortex 10 (2000) (12), pp. 1168–1175. Full Text via CrossRef
| View Record in Scopus | Cited By in Scopus (128)
Liddle, 2000 P.F. Liddle, Cognitive impairment in schizophrenia: its impact on social
functioning, Acta psychiatrica Scandinavica. Supplementum 400 (2000), pp. 11–16. View
Record in Scopus | Cited By in Scopus (55)
Lidow et al., 1991 M.S. Lidow, P.S. Goldman-Rakic, D.W. Gallager and P. Rakic,
Distribution of dopaminergic receptors in the primate cerebral cortex: quantitative
autoradiographic analysis using [3H]raclopride, [3H]spiperone and [3H]SCH23390,
Neuroscience 40 (1991), pp. 657–671. Abstract | PDF (4264 K) | View Record in Scopus |
Cited By in Scopus (133)
Lidow and Goldman-Rakic, 1994 M.S. Lidow and P.S. Goldman-Rakic, A common action of
clozapine, haloperidol, and remoxipride on D1- and D2-dopaminergic receptors in the
primate cerebral cortex, Proceedings of the National Academy of Sciences USA 91 (1994)
(10), pp. 4353–4356. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus
(102)
Lidow et al., 1997 M.S. Lidow, J.D. Elsworth and P.S. Goldman-Rakic, Down-regulation of
the D1 and D5 dopamine receptors in the primate prefrontal cortex by chronic treatment with
antipsycotic drugs, Journal of Pharmacology and Experimental Therapeutics 281 (1997) (1),
pp. 597–603. View Record in Scopus | Cited By in Scopus (74)
Lidow et al., 1998 M.S. Lidow, G.V. Williams and P.S. Goldman-Rakic, The cerebral cortex:
a case for a common site of action of antipsychotics, Trends in Pharmacological Sciences 19
(1998) (4), pp. 136–140. Article | PDF (136 K) | View Record in Scopus | Cited By in Scopus
(139)
Linn et al., 1999 G.S. Linn, R.T. O‘Keeffe, C.E. Schroeder, K. Lifshitz and D.C. Javitt,
Behavioral effects of chronic phencyclidine in monkeys, Neuroreport 10 (1999) (13), pp.
2789–2793 Erratum in: Neuroreport 2000 Mar 20;11(4):inside back cover, 901.. View
Record in Scopus | Cited By in Scopus (15)
Linn and Javitt, 2001 G.S. Linn and D.C. Javitt, Phencyclidine (PCP)-induced deficits of
prepulse inhibition in monkeys, Neuroreport 12 (2001) (1), pp. 117–120. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (34)
Linn et al., 2003 G.S. Linn, S.S. Negi, S.V. Gerum and D.C. Javitt, Reversal of
phencyclidine-induced prepulse inhibition deficits by clozapine in monkeys,
Psychopharmacology (Berl) 169 (2003) (3-4), pp. 234–239 Epub 2003 Jul 4.. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (40)
Lisman et al., 1998 J.E. Lisman, J.M. Fellous and X.J. Wang, A role for NMDA-receptor
channels in working memory, Nature Neuroscience 1 (1998) (4), pp. 273–275. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (148)
Ljungberg et al., 1991 T. Ljungberg, P. Apicella and W. Schultz, Responses of monkey
midbrain dopamine neurons during delayed alternation performance, Brain Research 567
(1991) (2), pp. 337–341. Abstract | PDF (422 K) | View Record in Scopus | Cited By in
Scopus (43)
Lysaker et al., 1996 P.H. Lysaker, M.D. Bell, S. Bioty and W.S. Zito, Performance on the
Wisconsin card sorting test as a predictor of rehospitalization in schizophrenia, Journal of
Nervous and Mental Disorders 184 (1996), pp. 319–321. Full Text via CrossRef | View
Record in Scopus | Cited By in Scopus (17)
Ma et al., 1999 S.Y. Ma, B.J. Ciliax, G. Stebbins, S. Jaffar, J.N. Joyce and E.J. Cochran et al.,
Dopamine transporter-immunoreactive neurons decrease with age in the human substantia
nigra, Journal of Comparative Neurology 409 (1999), pp. 25–37. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (74)
Marcus et al., 2005 M.M. Marcus, K.E. Jardemark, M.L. Wadenberg, X. Langlois, P. Hertel
and T.H. Svensson, Combined alpha2 and D2/3 receptor blockade enhances cortical
glutamatergic transmission and reverses cognitive impairment in the rat, International
Journal of Neuropsychopharmacology 8 (2005) (3), pp. 315–327 Epub 2005 Apr 7.. View
Record in Scopus | Cited By in Scopus (27)
Mathalon et al., 2002 D.H. Mathalon, M. Fedor, W.O. Faustman, M. Gray, N. Askari and
J.M. Ford, Response-monitoring dysfunction in schizophrenia: an event-related brain
potential study, Journal of Abnormal Psychology 111 (2002) (1), pp. 22–41. Abstract | Full
Text via CrossRef | View Record in Scopus | Cited By in Scopus (82)
Mattay et al., 2002 V.S. Mattay, A. Tessitore, J.H. Callicott, A. Bertolino, T.E. Goldberg and
T.N. Chase et al., Dopaminergic modulation of cortical function in patients with Parkinson‘s
disease, Annals of Neurology 51 (2002) (2), pp. 156–164. Full Text via CrossRef | View
Record in Scopus | Cited By in Scopus (171)
Mattay et al., 2003 V.S. Mattay, T.E. Goldberg, F. Fera, A.R. Hariri, A. Tessitore and M.F.
Egan et al., Catechol O-methyltransferase val158-met genotype and individual variation in
the brain response to amphetamine, Proceedings of the National Academy of Sciences USA
100 (2003) (10), pp. 6186–6191 Epub 2003 Apr 25. Full Text via CrossRef | View Record in
Scopus | Cited By in Scopus (329)
Maurice et al., 2001 N. Maurice, T. Tkatch, M. Meisler, L.K. Sprunger and D.J. Surmeier,
D1/D5 dopamine receptor activation differentially modulates rapidly inactivating and
persistent sodium currents in prefrontal cortex pyramidal neurons, Journal of Neuroscience
21 (2001) (7), pp. 2268–2277. View Record in Scopus | Cited By in Scopus (106)
McCormick et al., 2003 D.A. McCormick, Y. Shu, A. Hasenstaub, M. Sanchez-Vives, M.
Badoual and T. Bal, Persistent cortical activity: mechanisms of generation and effects on
neuronal excitability, Cerebral Cortex 13 (2003) (11), pp. 1219–1231. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (64)
McGurk and Meltzer, 2000 S.R. McGurk and H.Y. Meltzer, The role of cognition in
vocational functioning in schizophrenia, Schizophrenia Research 45 (2000) (3), pp. 175–184.
Article | PDF (100 K) | View Record in Scopus | Cited By in Scopus (134)
Millar and Armstrong-James, 1982 J. Millar and M. Armstrong-James, Dendrite spikes
recorded extracellularly from dorsal horn neurones, Brain Research 243 (1982) (2), pp. 253–
262. Abstract | PDF (780 K) | View Record in Scopus | Cited By in Scopus (1)
Miller et al., 1997 D.D. Miller, N.C. Andreasen, D.S. O‘Leary, K. Rezai, G.L. Watkins and
L.L. Ponto et al., Effect of antipsychotics on regional cerebral blood flow measured with
positron emission tomography, Neuropsychopharmacology 17 (1997) (4), pp. 230–240.
Abstract | Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (58)
Miller, 2000 E.K. Miller, The prefrontal cortex: no simple matter, Neuroimage 11 (2000) (5
Pt 1), pp. 447–450. Abstract | PDF (33 K) | View Record in Scopus | Cited By in Scopus (35)
Miller and Wang, 2006 P. Miller and X.J. Wang, Inhibitory control by an integral feedback
signal in prefrontal cortex: a model of discrimination between sequential stimuli, Proceedings
of the National Academy of Sciences USA 103 (2006) (1), pp. 201–206 Epub 2005 Dec 21..
Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (14)
Moghaddam et al., 1997 B. Moghaddam, B. Adams, A. Verma and D. Daly, Activation of
glutamatergic neurotransmission by ketamine: a novel step in the pathway from NMDA
receptor blockade to dopaminergic and cognitive disruptions associated with the prefrontal
cortex, Journal of Neuroscience 17 (1997) (8), pp. 2921–2927. View Record in Scopus |
Cited By in Scopus (436)
Moore et al., 2003 T.L. Moore, R.J. Killiany, J.G. Herndon, D.L. Rosene and M.B. Moss,
Impairment in abstraction and set shifting in aged rhesus monkeys, Neurobiology of Aging 24
(2003) (1), pp. 125–134. Article | PDF (270 K) | View Record in Scopus | Cited By in Scopus
(23)
Morrow et al., 2000 B.A. Morrow, R.H. Roth and J.D. Elsworth, TMT, a predator odor,
elevates mesoprefrontal dopamine metabolic activity and disrupts short-term working
memory in the rat, Brain Research Bulletin 52 (2000) (6), pp. 519–523. Article | PDF (114
K) | View Record in Scopus | Cited By in Scopus (64)
Murphy et al., 1996a B.L. Murphy, A.F. Arnsten, P.S. Goldman-Rakic and R.H. Roth,
Increased dopamine turnover in the prefrontal cortex impairs spatial working memory
performance in rats and monkeys, Proceedings of the National Academy of Sciences 93
(1996) (3), pp. 1325–1329. Full Text via CrossRef | View Record in Scopus | Cited By in
Scopus (322)
Murphy et al., 1996b B.L. Murphy, A.F. Arnsten, J.D. Jentsch and R.H. Roth, Dopamine and
spatial working memory in rats and monkeys: pharmacological reversal of stress-induced
impairment, Journal of Neuroscience 16 (1996) (23), pp. 7768–7775. View Record in Scopus
| Cited By in Scopus (127)
Narendran et al., 2005 R. Narendran, W.G. Frankle, R. Keefe, R. Gil, D. Martinez and M.
Slifstein et al., Altered prefrontal dopaminergic function in chronic recreational ketamine
users, American Journal of Psychiatry 162 (2005) (12), pp. 2352–2359. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (27)
Naoi and Maruyama, 1999 M. Naoi and W. Maruyama, Cell death of dopamine neurons in
aging and Parkinson‘s disease, Mechanisms of Ageing and Development 111 (1999), pp. 175–
178.
Ngan et al., 2002 E.T. Ngan, C.J. Lane, T.J. Ruth and P.F. Liddle, Immediate and delayed
effects of risperidone on cerebral metabolism in neuroleptic naive schizophrenic patients:
correlations with symptom change, Journal of Neurology, Neurosurgery, and Psychiatry 72
(2002) (1), pp. 106–110. Full Text via CrossRef | View Record in Scopus | Cited By in
Scopus (31)
Nieoullon, 2002 A. Nieoullon, Dopamine and the regulation of cognition and attention,
Progress In Neurobiology 67 (2002), pp. 53–83. Article | PDF (537 K) | View Record in
Scopus | Cited By in Scopus (268)
Nieuwenhuis et al., 2002 S. Nieuwenhuis, K.R. Ridderinkhof, D. Talsma, M.G. Coles, C.B.
Holroyd and A. Kok et al., A computational account of altered error processing in older age:
dopamine and the error-related negativity, Cognitive, Affective, and Behavioral Neuroscience
2 (2002) (1), pp. 19–36. Full Text via CrossRef | View Record in Scopus | Cited By in
Scopus (87)
Nystrom et al., 2000 L.E. Nystrom, T.S. Braver, F.W. Sabb, M.R. Delgado, D.C. Noll and
J.D. Cohen, Working memory for letters, shapes, and locations: fMRI evidence against
stimulus-based regional organization in human prefrontal cortex, Neuroimage 11 (2000) (5 Pt
1), pp. 424–446. Abstract | PDF (749 K) | View Record in Scopus | Cited By in Scopus (155)
Ogura and Aigner, 1993 H. Ogura and T.G. Aigner, MK-801 impairs recognition memory in
rhesus monkeys: comparison with cholinergic drugs, Journal of Pharmacology and
Experimental Therapeutics 266 (1993) (1), pp. 60–64. View Record in Scopus | Cited By in
Scopus (40)
Ongur and Price, 2000 D. Ongur and J.L. Price, The organization of networks within the
orbital and medial prefrontal cortex of rats, monkeys and humans, Cerebral Cortex 10 (2000)
(3), pp. 206–219. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (585)
Onn and Wang, 2005 S.P. Onn and X.B. Wang, Differential modulation of anterior cingulate
cortical activity by afferents from ventral tegmental area and mediodorsal thalamus,
European Journal of Neuroscience 21 (2005) (11), pp. 2975–2992. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (11)
O Scalaidhe et al., 1997 S.P. O Scalaidhe, F.A. Wilson and P.S. Goldman-Rakic, Areal
segregation of face-processing neurons in prefrontal cortex, Science 278 (1997) (5340), pp.
1135–1138. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (142)
Papadeas et al., 2004 S.T. Papadeas, B.L. Blake, D.J. Knapp and G.R. Breese, Sustained
extracellular signal-regulated kinase 1/2 phosphorylation in neonate 6-hydroxydopamine-
lesioned rats after repeated D1-dopamine receptor agonist administration: implications for
NMDA receptor involvement, Journal of Neuroscience 24 (2004) (26), pp. 5863–5876. Full
Text via CrossRef | View Record in Scopus | Cited By in Scopus (24)
Passingham, 1985 R.E. Passingham, Memory of monkeys (Macaca mulatta) with lesions in
prefrontal cortex, Behavioral Neuroscience 99 (1985) (1), pp. 3–21. Abstract | Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (72)
Paule, 1994 M.G. Paule, Acute behavioral toxicity of MK-801 and phencyclidine: effects on
rhesus monkey performance in an operant test battery, Psychopharmacology Bulletin 30
(1994) (4), pp. 613–621. View Record in Scopus | Cited By in Scopus (12)
Paulson et al., 1991 P.E. Paulson, D.M. Camp and T.E. Robinson, Time course of transient
behavioral depression and persistent behavioral sensitization in relation to regional brain
monoamine concentrations during amphetamine withdrawal in rats, Psychopharmacology
(Berl) 103 (1991) (4), pp. 480–492. Full Text via CrossRef | View Record in Scopus | Cited
By in Scopus (213)
Paulson and Robinson, 1995 P.E. Paulson and T.E. Robinson, Amphetamine-induced time-
dependent sensitization of dopamine neurotransmission in the dorsal and ventral striatum: a
microdialysis study in behaving rats, Synapse 19 (1995) (1), pp. 56–65. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (168)
Peters et al., 2004 Y. Peters, N.E. Barnhardt and P. O‘Donnell, Prefrontal cortical up states
are synchronized with ventral tegmental area activity, Synapse 52 (2004) (2), pp. 143–152.
Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (22)
Phillips et al., 2004 A.G. Phillips, S. Ahn and S.B. Floresco, Magnitude of dopamine release
in medial prefrontal cortex predicts accuracy of memory on a delayed response task, Journal
of Neuroscience 24 (2004) (2), pp. 547–553. Full Text via CrossRef | View Record in Scopus
| Cited By in Scopus (91)
Popke et al., 2001 E.J. Popke, R.R. Allen, E.C. Pearson, T.G. Hammond and M.G. Paule,
Differential effects of two NMDA receptor antagonists on cognitive—behavioral
performance in young nonhuman primates II, Neurotoxicology and Teratology 23 (2001) (4),
pp. 333–347. Article | PDF (358 K) | View Record in Scopus | Cited By in Scopus (17)
Pouzet et al., 1999 B. Pouzet, H. Welzl, M.K. Gubler, L. Broersen, C.L. Veenman and J.
Feldon et al., The effects of NMDA-induced retrohippocampal lesions on performance of
four spatial memory tasks known to be sensitive to hippocampal damage in the rat, European
Journal of Neuroscience 11 (1999) (1), pp. 123–140. Full Text via CrossRef | View Record
in Scopus | Cited By in Scopus (48)
Prieto-Gomez et al., 2005 B. Prieto-Gomez, A.M. Vazquez-Alvarez, J.L. Martinez-Pena, C.
Reyes-Vazquez, P.B. Yang and N. Dafny, Methylphenidate and amphetamine modulate
differently the NMDA and AMPA glutamatergic transmission of dopaminergic neurons in
the ventral tegmental area, Life Sciences 77 (2005) (6), pp. 635–649. View Record in Scopus |
Cited By in Scopus (3)
Priori et al., 1993 A. Priori, L. Bertolasi, J.C. Rothwell, B.L. Day and C.D. Marsden, Some
saccadic eye movements can be delayed by transcranial magnetic stimulation of the cerebral
cortex in man, Brain 116 (1993) (Pt 2), pp. 355–367. View Record in Scopus | Cited By in
Scopus (50)
Ramos et al., 2003 B.P. Ramos, S.G. Birnbaum, I. Lindenmayer, S.S. Newton, R.S. Duman
and A.F. Arnsten, Dysregulation of protein kinase a signaling in the aged prefrontal cortex:
new strategy for treating age-related cognitive decline, Neuron 40 (2003) (4), pp. 835–845.
Article | PDF (287 K) | View Record in Scopus | Cited By in Scopus (56)
Rao et al., 1997 S.C. Rao, G. Rainer and E.K. Miller, Integration of what and where in the
primate prefrontal cortex, Science 276 (1997) (5313), pp. 821–824. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (357)
Rao et al., 1999 S.G. Rao, G.V. Williams and P.S. Goldman-Rakic, Isodirectional tuning of
adjacent interneurons and pyramidal cells during working memory: evidence for
microcolumnar organization in PFC, Journal of Neurophysiology 81 (1999) (4), pp. 1903–
1916. View Record in Scopus | Cited By in Scopus (136)
Rao et al., 2000 S.G. Rao, G.V. Williams and P.S. Goldman-Rakic, Destruction and creation
of spatial tuning by disinhibition: GABA(A) blockade of prefrontal cortical neurons engaged
by working memory, Journal of Neuroscience 20 (2000), pp. 485–494. View Record in
Scopus | Cited By in Scopus (146)
Rapp and Amaral, 1989 P.R. Rapp and D.G. Amaral, Evidence for task-dependent memory
dysfunction in the aged monkey, Journal of Neuroscience 104 (1989), pp. 876–884.
Rinne et al., 1990 J.O. Rinne, P. Lonneberg and P. Marjamaki, Age-dependent decline in
human brain dopamine D1 and D2 receptors, Brain Research 508 (1990), pp. 349–352.
Abstract | PDF (368 K) | View Record in Scopus | Cited By in Scopus (68)
Roberts, 2006 A.C. Roberts, Primate orbitofrontal cortex and adaptive behaviour, Trends in
Cognitive Sciences 10 (2006) (2), pp. 83–90 Epub 2005 Dec 27.. Article | PDF (254 K) |
View Record in Scopus | Cited By in Scopus (33)
Robinson and Becker, 1986 T.E. Robinson and J.B. Becker, Enduring changes in brain and
behavior produced by chronic amphetamine administration: a review and evaluation of
animal models of amphetamine psychosis, Brain Research 396 (1986) (2), pp. 157–198.
Abstract | PDF (4740 K) | View Record in Scopus | Cited By in Scopus (554)
Robinson et al., 1985 T.E. Robinson, J.B. Becker, C.J. Moore, E. Castaneda and G.
Mittleman, Enduring enhancement in frontal cortex dopamine utilization in an animal model
of amphetamine psychosis, Brain Res. 343 (1985) (2), pp. 374–377. Abstract | PDF (349 K) |
View Record in Scopus | Cited By in Scopus (23)
Roesch and Olson, 2004 M.R. Roesch and C.R. Olson, Neuronal activity related to reward
value and motivation in primate frontal cortex, Science 304 (2004) (5668), pp. 307–310. Full
Text via CrossRef | View Record in Scopus | Cited By in Scopus (157)
Rolls, 2000 E.T. Rolls, The orbitofrontal cortex and reward, Cerebral Cortex 10 (2000) (3),
pp. 284–294. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (545)
Rowe et al., 2000 J.B. Rowe, I. Toni, O. Josephs, R.S. Frackowiak and R.E. Passingham, The
prefrontal cortex: response selection or maintenance within working memory?, Science 288
(2000) (5471), pp. 1656–1660. Full Text via CrossRef | View Record in Scopus | Cited By in
Scopus (378)
Rowland et al., 2005a L.M. Rowland, R.S. Astur, R.E. Jung, J.R. Bustillo, J. Lauriello and
R.A. Yeo, Selective cognitive impairments associated with NMDA receptor blockade in
humans, Neuropsychopharmacology 30 (2005) (3), pp. 633–639. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (35)
Rowland et al., 2005b L.M. Rowland, J.R. Bustillo, P.G. Mullins, R.E. Jung, R. Lenroot and
E. Landgraf et al., Effects of ketamine on anterior cingulate glutamate metabolism in healthy
humans: a 4-T proton MRS study, American Journal of Psychiatry 162 (2005) (2), pp. 394–
396. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (36)
Rupniak et al., 1991 N.M. Rupniak, N.A. Samson, M.J. Steventon and S.D. Iversen,
Induction of cognitive impairment by scopolamine and noncholinergic agents in rhesus
monkeys, Life Sciences 48 (1991) (9), pp. 893–899. Abstract | View Record in Scopus | Cited
By in Scopus (12)
Rushworth et al., 2004 M.F. Rushworth, M.E. Walton, Y.S.W. Kennerle and D.M.
Bannerman, Action sets and decisions in the medial frontal cortex, Trends in Cognitive
Sciences 8 (2004) (9), pp. 410–417. Article | PDF (243 K) | View Record in Scopus | Cited
By in Scopus (275)
Sawaguchi, 2001 T. Sawaguchi, The effects of dopamine and its antagonists on directional
delay-period activity of prefrontal neurons in monkeys during an oculomotor delayed-
response task, Neurosci Research 41 (2001) (2), pp. 115–128. Article | PDF (304 K) | View
Record in Scopus | Cited By in Scopus (47)
Sawaguchi and Goldman-Rakic, 1991 T. Sawaguchi and P.S. Goldman-Rakic, D1 dopamine
receptors in prefrontal cortex: involvement in working memory, Science 251 (1991), pp. 947–
950. View Record in Scopus | Cited By in Scopus (577)
Sawaguchi and Goldman-Rakic, 1994 T. Sawaguchi and P.S. Goldman-Rakic, The role of
D1-dopamine receptor in working memory: local injections of dopamine antagonists into the
prefrontal cortex of rhesus monkeys performing an oculomotor delayed-response task,
Journal of Neurophysiology 71 (1994) (2), pp. 515–528. View Record in Scopus | Cited By in
Scopus (307)
Schneider and Roeltgen, 1993 J.S. Schneider and D.P. Roeltgen, Delayed matching-to-
sample, object retrieval, and discrimination reversal deficits in chronic low dose MPTP-
treated monkeys, Brain Research 615 (1993) (2), pp. 351–354. Abstract | PDF (370 K) | View
Record in Scopus | Cited By in Scopus (41)
Schneider et al., 1994a J.S. Schneider, Z.Q. Sun and D.P. Roeltgen, Effects of dopamine
agonists on delayed response performance in chronic low-dose MPTP-treated monkeys,
Pharmacology, Biochemistry, and Behavior 48 (1994) (1), pp. 235–240. Abstract | PDF (654
K) | View Record in Scopus | Cited By in Scopus (28)
Schneider et al., 1994b J.S. Schneider, Z.Q. Sun and D.P. Roeltgen, Effects of dihydrexidine,
a full D-1 dopamine receptor agonist, on delayed response performance in chronic low dose
MPTP-treated monkeys, Brain Research 663 (1994) (1), pp. 140–144. Abstract | PDF (478
K) | View Record in Scopus | Cited By in Scopus (38)
Schneider and Pope-Coleman, 1995 J.S. Schneider and A. Pope-Coleman, Cognitive deficits
precede motor deficits in a slowly progressing model of parkinsonism in monkeys,
Neurodegeneration 4 (1995) (3), pp. 245–255. Article | PDF (1022 K) | View Record in
Scopus | Cited By in Scopus (59)
Schneider et al., 1999 J.S. Schneider, J.P. Tinker, M. Van Velson, F. Manzaghi and G.K.
Lloyd, Nicotinic acetylcholine receptor agonist SIB-1508Y improves cognitive functioning in
chronic low-dose MPTP-treated monkeys, Journal of Pharmacology and Experimental
Therapeutics 290 (1999) (2), pp. 731–739. View Record in Scopus | Cited By in Scopus (48)
Schneider et al., 2003 J.S. Schneider, J.P. Tinker, G. Menzaghi and G.K. Lloyd, The subtype-
selective nicotinic acetylcholine receptor agonist SIB-1553A improves both attention and
memory components of a spatial working memory task in chronic low dose 1-methyl-4-
phenyl-1,2,3,6-tetrahydropyridine-treated monkeys, Journal of Pharmacology and
Experimental Therapeutics 306 (2003) (1), pp. 401–406. Full Text via CrossRef | View
Record in Scopus | Cited By in Scopus (18)
Schultz et al., 1993 W. Schultz, P. Apicella and T. Ljungberg, Responses of monkey
dopamine neurons to reward and conditioned stimuli during successive steps of learning a
delayed response task, Journal of Neuroscience 13 (1993) (3), pp. 900–913. View Record in
Scopus | Cited By in Scopus (456)
Schultz et al., 2000 W. Schultz, L. Tremblay and J.R. Hollerman, Reward processing in
primate orbitofrontal cortex and basal ganglia, Cerebral Cortex 10 (2000) (3), pp. 272–284.
Scott et al., 2002 L. Scott, M.S. Kruse, H. Forssberg, H. Brismar, P. Greengard and A.
Aperia, Selective up-regulation of dopamine D1 receptors in dendritic spines by NMDA
receptor activation, Proceedings of the National Academy of Sciences USA 99 (2002) (3), pp.
1661–1664. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (76)
Scott et al., 2006 L. Scott, S. Zelenin, S. Malmersjo, J.M. Kowalewski, E.Z. Markus and A.C.
Nairn et al., Allosteric changes of the NMDA receptor trap diffusible dopamine 1 receptors in
spines, Proceedings of the National Academy of Sciences 103 (2006) (3), pp. 762–767. Full
Text via CrossRef | View Record in Scopus | Cited By in Scopus (38)
Seamans et al., 1997 J.K. Seamans, N.A. Gorelova and C.R. Yang, Contributions of voltage-
gated Ca2+ channels in the proximal versus distal dendrites to synaptic integration in
prefrontal cortical neurons, Journal of Neuroscience 17 (1997) (15), pp. 5936–5948. View
Record in Scopus | Cited By in Scopus (56)
Seamans et al., 2001 J.K. Seamans, D. Durstewitz, B.R. Christie, C.F. Stevens and T.J.
Sejnowski, Dopamine D1/D5 receptor modulation of excitatory synaptic inputs to layer V
prefrontal cortex neurons, Proceedings of the National Academy of Sciences USA 98 (2001)
(1), pp. 301–306. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (177)
Selemon et al., 2006 L.D. Selemon, A. Begovic, P.S. Goldman-Rakic and S.A. Castner,
Amphetamine sensitization alters dendritic morphology in prefrontal cortical pyramidal
neurons in the non-human primate, Neuropsychopharmacology (2006) [Epub ahead of print].
Selemon and Goldman-Rakic, 1988 L.D. Selemon and P.S. Goldman-Rakic, Common
cortical and subcortical targets of the dorsolateral prefrontal and posterior parietal cortices in
the rhesus monkey: evidence for a distributed neural network subserving spatially guided
behavior, Journal of Neuroscience 8 (1988) (11), pp. 4049–4068. View Record in Scopus |
Cited By in Scopus (294)
Selemon and Rajkowska, 2003 L.D. Selemon and G. Rajkowska, Cellular pathology in the
dorsolateral prefrontal cortex distinguishes schizophrenia from bipolar disorder, Current
Molecular Medicine 3 (2003) (5), pp. 427–436. Full Text via CrossRef | View Record in
Scopus | Cited By in Scopus (31)
Selemon et al., 1995 L.D. Selemon, G. Rajkowska and P.S. Goldman-Rakic, Abnormally
high neuronal density in the schizophrenic cortex. A morphometric analysis of prefrontal area
9 and occipital area 17, Archives of General Psychiatry 52 (1995) (10), pp. 805–818.
Shelley et al., 1999 A.M. Shelley, G. Silipo and D.C. Javitt, Diminished responsiveness of
ERPs in schizophrenic subjects to changes in auditory stimulation parameters: implications
for theories of cortical dysfunction, Schizophrenia Research 37 (1999) (1), pp. 65–79. Article
| PDF (246 K) | View Record in Scopus | Cited By in Scopus (81)
Shu et al., 2003 Y. Shu, A. Hasenstaub and D.A. McCormick, Turning on and off recurrent
balanced cortical activity, Nature 423 (2003) (6937), pp. 288–293. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (231)
Shu et al., 2006 Y. Shu, A. Hasenstaub, A. Duque, Y. Yu and A.D. McCormick, Modulation
of intracortical synaptic potentials by presynaptic somatic membrane potential, Nature 441
(2006) (7094), pp. 761–765. Full Text via CrossRef | View Record in Scopus | Cited By in
Scopus (68)
Smith et al., 1999a T.E. Smith, J.W. Hull, S. Romanelli, E. Fertuck and K.A. Weiss,
Symptoms and neurocognition as rate limiters in skills training for psychotic patients,
American Journal of Psychiatry 156 (1999) (11), pp. 1817–1818. View Record in Scopus |
Cited By in Scopus (41)
Smith et al., 1999b T.E. Smith, J.W. Hull, M. Goodman, A. Hedayat-Harris, D.F. Willson
and L.M. Israel et al., The relative influence of symptoms, insight, and neurocognition on
social adjustment in schizophrenia and schizoaffective disorder, Journal of Nervous and
Mental Disorders 187 (1999) (2), pp. 102–108. Full Text via CrossRef | View Record in
Scopus | Cited By in Scopus (108)
Smith-Roe and Kelley, 2000 S.L. Smith-Roe and A.E. Kelley, Coincident activation of
NMDA and dopamine D1 receptors within the nucleus accumbens core is required for
appetitive instrumental learning, Journal of Neuroscience 20 (2000) (20), pp. 7737–7742.
View Record in Scopus | Cited By in Scopus (139)
Snyder, 1973 S.H. Snyder, Amphetamine psychosis: a ―model‖ of schizophrenia mediated by
catecholamines, Am. J. Psychiatry 130 (1973) (1), pp. 61–67. View Record in Scopus | Cited
By in Scopus (127)
Snyder et al., 1998 G.L. Snyder, A.A. Fienberg, R.L. Huganir and P. Greengard, A
dopamine/D1 receptor/protein kinase A/dopamine- and cAMP-egulated phosphoprotein (Mr
32 kDa)/protein phosphatase-1 pathway regulates dephosphorylation of the NMDA receptor,
Journal of Neuroscience 18 (1998) (24), pp. 10297–10303. View Record in Scopus | Cited
By in Scopus (177)
Steinpresis, 1996 R.E. Steinpresis, The behavioral and neurochemical effects of phenyclidine
in humans and animals: some implications for modeling psychosis, Behavioral Brain
Research 74 (1996) (1-2), pp. 45–55.
Stewart and Vezina, 1989 J. Stewart and P. Vezina, Microinjections of Sch-23390 into the
ventral tegmental area and substantia nigra pars reticulata attenuate the development of
sensitization to the locomotor activating effects of systemic amphetamine, Brain Research
495 (1989) (2), pp. 401–406. Abstract | PDF (493 K) | View Record in Scopus | Cited By in
Scopus (116)
Stoet and Snyder, 2006 G. Stoet and L.H. Snyder, Effects of the NMDA antagonist ketamine
on task-switching performance: evidence for specific impairments of executive control,
Neuropsychopharmacology 31 (2006) (8), pp. 1675–1681 Epub 2005 Oct 5.. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (9)
Sun et al., 2005 X. Sun, Y. Zhao and M.E. Wolf, Dopamine receptor stimulation modulates
AMPA receptor synaptic insertion in prefrontal cortex neurons, Journal of Neuroscience 25
(2005) (32), pp. 7342–7351. Full Text via CrossRef | View Record in Scopus | Cited By in
Scopus (70)
Surmeier et al., 1995 D.J. Surmeier, J. Bargas, H.C. Hemmings Jr., A.C. Nairn and P.
Greengard, Modulation of calcium currents by a D1 dopaminergic protein kinase/phosphatase
cascade in rat neostriatal neurons, Neuron 14 (1995) (2), pp. 385–397. Article | PDF (1460
K) | View Record in Scopus | Cited By in Scopus (309)
Suzuki and Azuma, 1983 H. Suzuki and M. Azuma, Topographic studies on visual neurons in
the dorsolateral prefrontal cortex of the monkey, Experimental Brain Research 53 (1983) (1),
pp. 47–58. View Record in Scopus | Cited By in Scopus (38)
Taffe et al., 2002a M.A. Taffe, M.R. Weed, T. Gutierrez, S.A. Davis and L.H. Gold,
Differential muscarinic and NMDA contributions to visuo-spatial paired-associate learning in
rhesus monkeys, Psychopharmacology (Berl) 160 (2002) (3), pp. 253–262. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (25)
Taffe et al., 2002b M.A. Taffe, S.A. Davis, T. Gutierrez and L.H. Gold, Ketamine impairs
multiple cognitive domains in rhesus monkeys, Drug and Alcohol Dependence 68 (2002) (2),
pp. 175–187. Article | PDF (252 K) | View Record in Scopus | Cited By in Scopus (26)
Tamminga, 1998 C.A. Tamminga, Schizophrenia and glutamatergic transmission, Critical
Reviews in Neurobiology 12 (1998) (1-2), pp. 21–36. View Record in Scopus | Cited By in
Scopus (234)
Tamminga et al., 1995 C.A. Tamminga, H.H. Holcomb, X.M. Gao and A.C. Lahti, Glutamate
pharmacology and the treatment of schizophrenia: current status and future directions,
International Clinical Psychopharmacology 10 (1995) (Suppl 3), pp. 29–37. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (47)
Thierry et al., 1973 A.M. Thierry, G. Blanc, A. Sobel, L. Stinus and J. Golwinski,
Dopaminergic terminals in the rat cortex, Science 182 (1973) (4111), pp. 499–501. View
Record in Scopus | Cited By in Scopus (62)
Tiesinga et al., 2004 P.H. Tiesinga, J.M. Fellous, E. Salinas, J.V. Jose and T.J. Sejnowski,
Inhibitory synchrony as a mechanism for attentional gain modulation, Journal of Physiology
Paris 98 (2004) (4-6), pp. 296–314 Epub 2005 Nov 7.. Article | PDF (671 K) | View Record
in Scopus | Cited By in Scopus (29)
Tseng and O‘Donnell, 2004 K.Y. Tseng and P. O‘Donnell, Dopamine-glutamate interactions
controlling prefrontal cortical pyramidal cell excitability involve multiple signaling
mechanisms, Journal of Neuroscience 24 (2004) (22), pp. 5131–5139. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (106)
Tseng et al., 2006 K.Y. Tseng, N. Mallet, K.L. Toreson, C. Le Moine, F. Gonon and P.
O‘Donnell, Excitatory response of prefrontal cortical fast-spiking interneurons to ventral
tegmental area stimulation in vivo, Synapse 59 (2006) (7), pp. 412–417. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (28)
Tsukada et al., 2005a H. Tsukada, S. Nishiyama, D. Fukumoto, K. Sato, T. Kakiuchi and E.F.
Domino, Chronic NMDA antagonism impairs working memory, decreases extracellular
dopamine, and increases D1 receptor binding in prefrontal cortex of conscious monkeys,
Neuropsychopharmacology 30 (2005) (10), pp. 1861–1869. Full Text via CrossRef | View
Record in Scopus | Cited By in Scopus (28)
Tsukada et al., 2005b H. Tsukada, K. Miyasato, S. Nishiyama, D. Fukumoto, T. Kakiuchi and
E.F. Domino, Nicotine normalizes increased prefrontal cortical dopamine D1 receptor
binding and decreased working memory performance produced by repeated pretreatment with
MK-801: a PET study in conscious monkeys, Neuropsychopharmacology 30 (2005) (12), pp.
2144–2153. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (16)
Ungerleider and Haxby, 1994 L.G. Ungerleider and J.V. Haxby, ‘What‘ and ‘where‘ in the
human brain, Current Opinions in Neurobiology 4 (1994) (2), pp. 157–165. Article | PDF
(1293 K) | View Record in Scopus | Cited By in Scopus (540)
Valjent et al., 2005 E. Valjent, V. Pascoli, P. Svenningsson, S. Paul, H. Enslen and J.C.
Corvol et al., Regulation of a protein phosphatase cascade allows convergent dopamine and
glutamate signals to activate ERK in the striatum, Proceedings of the National Academy of
Sciences USA 102 (2005) (2), pp. 491–496. Full Text via CrossRef | View Record in Scopus |
Cited By in Scopus (153)
Vezina and Stewart, 1989 P. Vezina and J. Stewart, The effect of dopamine receptor blockade
on the development of sensitization to the locomotor activating effects of amphetamine and
morphine, Brain Research 499 (1989) (1), pp. 108–120. Abstract | PDF (1071 K) | View
Record in Scopus | Cited By in Scopus (143)
Volkow et al., 1998 N.D. Volkow, R.C. Gur, G.J. Wang, J.S. Fowler, P.J. Moberg and Y.S.
Ding et al., Association between decline in brain dopamine activity with age and cognitive
and motor impairment in healthy individuals, American Journal of Psychiatry 155 (1998), pp.
344–349. View Record in Scopus | Cited By in Scopus (304)
Vollenweider et al., 1997a F.X. Vollenweider, K.L. Leenders, C. Scharfetter, A. Antonini, P.
Maguire and J. Missimer et al., Metabolic hyperfrontality and psychopathology in the
ketamine model of psychosis using positron emission tomography (PET)
[18F]fluorodeoxyglucose (FDG), European Neuropsychopharmacology 7 (1997) (1), pp. 9–
24. Article | PDF (1786 K) | View Record in Scopus | Cited By in Scopus (124)
Vollenweider et al., 1997b F.X. Vollenweider, K.L. Leenders, I. Oye, D. Hell and J. Angst,
Differential psychopathology and patterns of cerebral glucose utilisation produced by (S)-
and (R)-ketamine in healthy volunteers using positron emission tomography (PET), European
Neuropsychopharmacology 7 (1997) (1), pp. 25–38. Article | PDF (3858 K) | View Record in
Scopus | Cited By in Scopus (95)
Waelti et al., 2001 P. Waelti, A. Dickinson and W. Schultz, Dopamine responses comply
with basic assumptions of formal learning theory, Nature 412 (2001) (6842), pp. 43–48. Full
Text via CrossRef | View Record in Scopus | Cited By in Scopus (270)
Walker, 1940 A.E. Walker, A cytoarchitectural study of the prefrontal area of the macaque
monkey, Journal of Comparative Neurology 73 (1940), pp. 59–86. Full Text via CrossRef
Wang, 1999 X.J. Wang, Synaptic basis of cortical persistent activity: the importance of
NMDA receptors to working memory, Journal of Neuroscience 19 (1999) (21), pp. 9587–
9603. View Record in Scopus | Cited By in Scopus (217)
Wang et al., 1998 Y. Wang, G.L. Chan, J.E. Holden, T. Dobko, E. Mak and M. Schulzer et
al., Age-dependent decline in dopamine D1 receptors in human brain: a PET study, Synapse
30 (1998), pp. 56–61. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus
(70)
Watanabe, 1996 M. Watanabe, Reward expectancy in primate prefrontal neurons, Nature 382
(1996) (6592), pp. 629–632. Full Text via CrossRef | View Record in Scopus | Cited By in
Scopus (345)
Watanabe et al., 2005 M. Watanabe, K. Hikosaka, M. Sakagami and S. Shirakawa,
Functional significance of delay-period activity of primate prefrontal neurons in relation to
spatial working memory and reward/omission-of-reward expectancy, Experimental Brain
Research 166 (2005) (2), pp. 263–276 Epub 2005 Jul 21.. Full Text via CrossRef | View
Record in Scopus | Cited By in Scopus (9)
Weinberger et al., 1988 D.R. Weinberger, K.F. Berman and B.P. Illowsky, Physiological
dysfunction of dorsolateral prefrontal cortex in schizophrenia. III. A new cohort and evidence
for a monoaminergic mechanism, Archives of General Psychiatry 45 (1988) (7), pp. 609–615.
View Record in Scopus | Cited By in Scopus (288)
Weinberger et al., 2001 D.R. Weinberger, M.F. Egan, A. Bertolino, J.H. Callicott, V.S.
Mattay and B.K. Lipska et al., Prefrontal neurons and the genetics of schizophrenia,
Biological Psychiatry 50 (2001), pp. 825–844. Article | PDF (143 K) | View Record in
Scopus | Cited By in Scopus (383)
West and Grace, 2002 A.R. West and A.A. Grace, Opposite influences of endogenous
dopamine D1 and D2 receptor activation on activity states and electrophysiological properties
of striatal neurons: studies combining in vivo intracellular recordings and reverse
microdialysis, Journal of Neuroscience 22 (2002) (1), pp. 294–304. View Record in Scopus |
Cited By in Scopus (116)
Williams and Goldman-Rakic, 1995 G.V. Williams and P.S. Goldman-Rakic, Modulation of
memory fields by dopamine D1 receptors in prefrontal cortex, Nature 376 (1995) (6541), pp.
549–550.
Williams and Castner, 2006 G.V. Williams and S.A. Castner, Under the curve: critical issues
for elucidating D1 receptor function in working memory, Neuroscience 139 (2006) (1), pp.
263–276. Article | PDF (222 K) | View Record in Scopus | Cited By in Scopus (67)
Williams and Goldman-Rakic, 1998 S.M. Williams and P.S. Goldman-Rakic, Widespread
origin of the primate mesofrontal dopamine system, Cerebral Cortex 8 (1998) (4), pp. 321–
345. Full Text via CrossRef
Williams and Millar, 1990a G.V. Williams and J. Millar, Concentration-dependent actions of
stimulated dopamine release on neuronal activity in rat striatum, Neuroscience 39 (1990) (1),
pp. 1–16. Abstract | PDF (1970 K) | View Record in Scopus | Cited By in Scopus (43)
Williams and Millar, 1990b G.V. Williams and J. Millar, Differential actions of endogenous
and iontophoretic dopamine in rat striatum, European Journal of Neuroscience 2 (1990) (7),
pp. 658–661. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (15)
Wilson and Kawaguchi, 1996 C.J. Wilson and Y. Kawaguchi, The origins of two-state
spontaneous membrane potential fluctuations of neostriatal spiny neurons, Journal of
Neuroscience 16 (1996) (7), pp. 2397–2410. View Record in Scopus | Cited By in Scopus
(316)
Wilson et al., 1993 F.A. Wilson, S.P. Scalaidhe and P.S. Goldman-Rakic, Dissociation of
object and spatial processing domains in primate prefrontal cortex, Science 260 (1993)
(5116), pp. 1955–1958. View Record in Scopus | Cited By in Scopus (665)
Winterer et al., 2006 G. Winterer, F. Musso, G. Vucurevic, P. Stoeter, A. Konrad and B.
Seker et al., COMT genotype predicts BOLD signal and noise characteristics in prefrontal
circuits, Neuroimage (2006) [Epub ahead of print].
Wolf and Khansa, 1991 M.E. Wolf and M.R. Khansa, Repeated administration of MK-801
produces sensitization to its own locomotor stimulant effects but blocks sensitization to
amphetamine, Brain Research 562 (1991) (1), pp. 164–168. Abstract | PDF (431 K) | View
Record in Scopus | Cited By in Scopus (149)
Wolf et al., 1993 M.E. Wolf, F.J. White and X.T. Hu, Behavioral sensitization to MK-801
(dizocilpine): neurochemical and electrophysiological correlates in the mesoaccumbens
dopamine system, Behavioral Pharmacology 4 (1993) (4), pp. 429–442. View Record in
Scopus | Cited By in Scopus (51)
Wolf and Xue, 1999 M.E. Wolf and C.J. Xue, Amphetamine-induced glutamate efflux in the
rat ventral tegmental area is prevented by MK-801, SCH 23390, and ibotenic acid lesions of
the prefrontal cortex, Journal of Neurochemistry 73 (1999) (4), pp. 1529–1538. Full Text via
CrossRef | View Record in Scopus | Cited By in Scopus (44)
Wurtz and Goldberg, 1972 R.H. Wurtz and M.E. Goldberg, Activity of superior colliculus in
behaving monkey. 3. Cells discharging before eye movements, Journal of Neurophysiology
35 (1972) (4), pp. 575–586. View Record in Scopus | Cited By in Scopus (158)
Xue et al., 1996 C.J. Xue, J.P. Ng, Y. Li and M.E. Wolf, Acute and repeated systemic
amphetamine administration: effects on extracellular glutamate, aspartate, and serine levels in
rat ventral tegmental area and nucleus accumbens, Journal of Neurochemistry 67 (1996) (1),
pp. 352–363. View Record in Scopus | Cited By in Scopus (125)
Yang and Seamans, 1996 C.R. Yang and J.K. Seamans, Dopamine D1 receptor actions in
layers V–VI rat prefrontal cortex neurons in vitro: modulation of dendritic-somatic signal
integration, Journal of Neuroscience 16 (1996) (5), pp. 1922–1935. View Record in Scopus |
Cited By in Scopus (205)
Yang et al., 1999 C.R. Yang, J.K. Seamans and N. Gorelova, Developing a neuronal model
for the pathophysiology of schizophrenia based on the nature of electrophysiological actions
of dopamine in the prefrontal cortex, Neuropsychopharmacology 21 (1999) (2), pp. 161–194.
Article | PDF (489 K) | Full Text via CrossRef | View Record in Scopus | Cited By in Scopus
(114)
Young and Yang, 2004 C.E. Young and C.R. Yang, Dopamine D1/D5 receptor modulates
state-dependent switching of soma-dendritic Ca2+ potentials via differential protein kinase A
and C activation in rat prefrontal cortical neurons, Journal of Neuroscience 24 (2004) (1), pp.
8–23. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (34)
Young and Yang, 2005 C.E. Young and C.R. Yang, Dopamine D1-like receptor modulates
layer- and frequency-specific short-term synaptic plasticity in rat prefrontal cortical neurons,
European Journal of Neuroscience 21 (2005) (12), pp. 3310–3320. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (10)
Youngren et al., 1999 K.D. Youngren, F.M. Inglis, P.J. Pivirotto, H.P. Jedema, C.W.
Bradberry and P.S. Goldman-Rakic et al., Clozapine preferentially increases dopamine
release in the rhesus monkey prefrontal cortex compared with the caudate nucleus,
Neuropsychopharmacology 20 (1999) (5), pp. 403–412. Article | PDF (1927 K) | Full Text
via CrossRef | View Record in Scopus | Cited By in Scopus (55)
Zirnheld et al., 2004 P.J. Zirnheld, C.A. Carroll, P.D. Kieffaber, B.F. O‘Donnell, A. Shekhar
and W.P. Hetrick, Haloperidol impairs learning and error-related negativity in humans,
Journal of Cognitive Neuroscience 16 (2004) (6), pp. 1098–1112. Full Text via CrossRef |
View Record in Scopus | Cited By in Scopus (42)