Dopamine stimulants

Swerdlow, N.R. Swanson, L.W. and Koob, G.F. Substantia innominata Critical link in the behavioral expression of mesolimbic dopamine stimulation in the rat. Neurosci Lett 50 19-24, 1984. [Pg.125]

Li+, at therapeutically relevant concentrations, is a potent inhibitor of norepinephrine-stimulated adenylate cyclase activity ex vivo in both rat [133] and human brain [134], and it inhibits norepinephrine-stimulated cAMP accumulation in Li+-treated patients. Li+ also inhibits dopamine-stimulated cAMP accumulation in rat brain [135]. These inhibitory effects of Li+ have been shown to be region specific within rat brain, a fact that has obvious significance for a therapeutic mechanism of action. It is interesting that other antimanic drugs may also have dampening effects on dopaminergic neurotransmission. [Pg.26]

Dopamine-Stimulating Medications. A variety of drugs that increase the availability of dopamine have been studied in cocaine addicts including L-DOPA, bupropion, amantadine, and methylphenidate. In small uncontrolled trials, these have shown some benefit, but definitive studies have yet to be performed. In addition, some dopamine-stimulating medications (in particular, the stimulants like methylphenidate or the amphetamines) are themselves subject to abuse, though, of note, this is typically not a problem when they are prescribed to patients who do not have a history of substance abuse such as, for example, in the treatment of attention deficit-hyperactivity disorder. [Pg.199]

Dopamine stimulates dopaminergic (DAi), and O -adrenoceptors. Accordingly, it is an inotropic agent that may also stimulate the kidney function. In higher doses, dopamine may cause vasoconstriction as a result of i-adrenoceptor stimulation. Dobutamine and dopamine may be combined, although this combination is hardly rational. [Pg.338]

Both stimulant users and smokers may down-regulate their dopamine receptors because of excessive dopamine stimulation. However, nicotine users may up-regulate their nicotinic cholinergic receptors to help compensate for the fact that nicotine keeps turning them off (Fig. 13—20). These possible changes in dopamine and nicotine receptors may be related to the psychopharmacological mechanisms underlying nicotine s profound ability to produce dependence and withdrawal. [Pg.519]

Dopamine stimulates dopamine, a-, and [3-adrenergic receptors. The use of dopamine in congestive heart failure is limited because it causes nausea and vomiting, becomes inactive when given orally, increases afterload (a-adrenergic receptor-mediated peripheral vasoconstriction), and enhances oxygen demand on the left ventricle. [Pg.363]

Though psilocybin is known as a natural hallucinogen and has a reputation of being gentler than LSD, it is still known to cause panic attacks, bad trips, and to precipitate mental illness in some people. In 1998, a study at the Psychiatric University Hospital in Zurich, Switzerland, demonstrated that psilocybin produces a psychosis-like syndrome in healthy humans that is similar to early schizophrenia. The study showed that psilocybin-induced psychosis was due to serotonin-2A receptor activation and was not dependent on dopamine stimulation. [Pg.430]

The evidence supporting the existence of a specific category of dopamine receptor on the parenchymal cells of the bovine parathyroid gland and the possible biochemical mechanisms by which dopamine stimulates the release of parathyroid hormone are reviewed. The dopamine receptor on the bovine parathyroid cell is compared to other dopamine receptors. [Pg.2]

The cellular and molecular events involved in the dopamine-stimulated release of PTH can be clarified in experiments utilizing bovine parathyroid cells dispersed with collagenase and DNase (ft). This dispersion procedure yields parenchymal cells with only a slight contamination by red blood cells. The parenchymal cells exclude trypan blue and appear normal by light and electron microscopy (ft). These cells release PTH in a linear fashion for several hours the release is inhibited by calcium and stimulated by dopamine and beta-adrenergic agonists at concentrations comparable to those used to elicit physiological responses in vivo (ft,ft). [Pg.3]

Like the dopamine-stimulated enhancement of PTH release, the dopamine-stimulated increase in cAMP content is maximal after 5 to 10 minutes of exposure to 10 uM dopamine (ft) and... [Pg.3]

Dopamine Stimulates Adenylate Cvclase Activity of Dispersed Bovine Parathyroid Cells... [Pg.6]

In either the presence or absence of GTP, half-maximal stimulation of enzyme activity is achieved with 3 uM dopamine. Both 6,7-ADTM and epinine (K-methyl dopamine) stimulate adenylate cyclase activity to the same degree as does dopamine (Figure 8). In contrast, apomorphine is a partial agonist eliciting only 30 of the maximal effect of dopamine. The dopamine-stimulated adenylate cyclase activity is selectively blocked by cis-flupenthixol rather than the trans-isomer of this antagonist (JJL). Among the antagonists tested, the order of potency is cis-flupenthixol = fluphenazine > chlorpromazine > haloperidol > trans-flupenthixol (Table I). [Pg.6]

Figure 7. Dopamine-stimulated adenylate cyclase activity in lysates of bovine parathyroid cells in the absence (Q) or presence (O) of 100 pM. guanosine triphosphate (GTP). (Reproduced with permission from Ref. 11. Copyright 1980, The...

The dopamine-stimulated formation of cAMP may initiate the dopamine-induced release of IR-PTH. A linear relationship exists between the dopamine-induced release of IR-PTH and the logarithm of the dopamine-induced accumulation of cAMP (17). Similarly, other agents increasing cAMP accumulation and IR-PTH release (e.g. beta-adrenergic agonists, secretin and phosphodiesterase inhibitors, also display such a log-linear relationship. Additional support for the possibility that intracellular cAMP might initiate PTH secretion comes from the observations that cholera toxin (JJ.), phosphodiesterase inhibitors (17) and dibutyryl cAMP (18), agents known to increase intracellular cAMP or mimic the biochemical effects of cAMP, increase the release of IR-PTH. [Pg.11]

Receptors Inhibiting Dopamine-stimulated oAHP Accumulation and... [Pg.13]

A schematic representation of the cellular mechanisms through which agonists, such as dopamine, stimulate PTH release and calcium inhibits hormonal secretion is shown in Figure 11. In this schema, cAMP is a stimulatory second messenger while cytosolic calcium serves to inhibit hormone release by acting at several loci within the cell. The detailed molecular mechanisms through which cAMP and cellular calcium modulate cellular function remain to be determined. [Pg.15]

Effects of dopaminergic antagonists on dopamine-stimulated cAMP accumulation, adenylate cyclase activity, and calmodulin-stimulated phosphodiesterase (PDE) activity in intact bovine parathyroid cells or cellular homogenates. Values for or IC50 are given as uM. NT, not tested. [Pg.17]

Secondly ergot derivatives which reveal a clearcut agonistic activity on prolactin secretion and as antiparkinson agents (20) were inactive on the cyclase. Surprisingly, lisuride and lergotrile were found to be weak antagonists of dopamine stimulated cAMP accumulation, but they could also antagonize the cAMP production stimulated by isoproterenol as... [Pg.27]

It is very likely an inaccuracy to call the D-l dopamine receptor an enzyme. Because of the effects of guanine nucleotides on dopamine-stimulated adenylate cyclase, it is likely by analogy with other receptors (i.e. the 3 receptor) that the D-l receptor is a distinct molecular entity which is coupled to adenylate cyclase by a guanine nucleotide binding subunit. Proof of this point, of course, will require physical separation of these entities. [Pg.32]

Dopamine can thus be added to the list of hormones and neurotransmitters which can stimulate or inhibit cyclic AMP formation, depending upon their tissue of action. Thus, while dopamine stimulates cyclic AMP formation in parathyroid cells, superior cervical ganglia, retina and striatal tissue (27, 58-61), it inhibits the accumulation of the cyclic nucleotide in cells of the intermediate and anterior lobes of the pituitary gland. Opposite effects on the cyclic AMP system are also found with LHRH which stimulates and inhibits cyclic AMP levels in the anterior pituitary gland (62) and ovary (63), respectively. Similarly, alpha-adrenergic agents show opposite effects on cyclic AMP formation in brain (64) and platelets (65). PGE, stimulates cyclic AMP formation in the anterior pituitary gland (62) while it inhibits the same parameter in fat cells (66). [Pg.60]

Figure 6. Potentiation by (—)-sulpiride of the dopamine stimulated efflux of cAMP from blocks of rat neostriatum. The efflux of cAMP from neostriatal tissue, stimulated with the indicated concentrations of dopamine, was estimated in the absence (M) and presence (O) of 50 j M (-)-sulpiride. (Reproduced with permission from Ref. 96. Copyright, Elsevier Biomedical Press.)...

Barnett, J., Kuczenski, R. (1986). Desensitization of rat striatal dopamine-stimulated adenylate cyclase after acute amphetamine administration. Journal of Pharmacology and Experimental Therapeutics, 237, 820—825. [Pg.467]

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