Jump to content

Template:Psychostimulant addiction: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
recoloring transcription factors + centering annotations
m c
Line 2: Line 2:
<center>This annotated image template is intended for transcluding to a variety of psychostimulant and addiction articles, as well as those on related protein topics.<br />The image file is located at '''[[COMMONS:File:ΔFosB.svg]]''' and a reusable version of this image is located at '''[[COMMONS:File:Annotated ΔFosB.svg screenshot.png]]'''.</center>{{documentation}}</noinclude>{{Annotated image 4
<center>This annotated image template is intended for transcluding to a variety of psychostimulant and addiction articles, as well as those on related protein topics.<br />The image file is located at '''[[COMMONS:File:ΔFosB.svg]]''' and a reusable version of this image is located at '''[[COMMONS:File:Annotated ΔFosB.svg screenshot.png]]'''.</center>{{documentation}}</noinclude>{{Annotated image 4
| nolink = yes
| nolink = yes
| caption = {{{caption|This diagram depicts the signaling events in the [[Mesolimbic pathway|brain's reward center]] that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like {{if pagename | Amphetamine = amphetamine| other = [[amphetamine]]}}, {{if pagename| Methylphenidate = methylphenidate| other = [[methylphenidate]]}}, and {{if pagename | Phenethylamine = phenethylamine| other = [[phenethylamine]]}}. Following presynaptic {{if pagename| Dopamine = dopamine| other = [[dopamine]]}} and [[glutamate]] [[cotransmission|co-release]] by such psychostimulants,<ref name="Glutamate-dopamine cotransmission review">{{vcite2 journal | vauthors = Broussard JI | title = Co-transmission of dopamine and glutamate | journal = J. Gen. Physiol. | volume = 139 | issue = 1 | pages = 93–96 | date = January 2012 | pmid = 22200950 | pmc = 3250102 | doi = 10.1085/jgp.201110659 | quote = <!-- Coincident and convergent input often induces plasticity on a postsynaptic neuron. The {{abbr|NAc|nucleus accumbens}} integrates processed information about the environment from basolateral amygdala, hippocampus, and prefrontal cortex (PFC), as well as projections from midbrain dopamine neurons. Previous studies have demonstrated how dopamine modulates this integrative process. For example, high frequency stimulation potentiates hippocampal inputs to the NAc while simultaneously depressing PFC synapses (Goto and Grace, 2005). The converse was also shown to be true; stimulation at PFC potentiates PFC–NAc synapses but depresses hippocampal–NAc synapses. In light of the new functional evidence of midbrain dopamine/glutamate co-transmission (references above), new experiments of NAc function will have to test whether midbrain glutamatergic inputs bias or filter either limbic or cortical inputs to guide goal-directed behavior. -->}}</ref><ref name="Glutamate-dopamine cotransmission review 2">{{vcite2 journal | vauthors = Descarries L, Berube-Carriere N, Riad M, Bo GD, Mendez JA, Trudeau LE | title = Glutamate in dopamine neurons: synaptic versus diffuse transmission | journal = Brain Res. Rev. | volume = 58 | issue = 2 | pages = 290–302 | date = August 2008 | pmid = 18042492 | doi = 10.1016/j.brainresrev.2007.10.005 | quote = <!-- Moreover, all {{abbr|TH|tyrosine hydroxylase}} varicosities which co-localize VGluT2 are synaptic, as if there was a link between the potential of {{abbr|DA|dopamine}} axon terminals to release glutamate and their establishment of synaptic junctions. Together with the RT-PCR and in situ hybridization data demonstrating the co-localization of TH and VGluT2 mRNA in mesencephalic neurons of the {{abbr|VTA|ventral tegmental area}}, these observations raise a number of fundamental questions regarding the functioning of the meso-telencephalic DA system in healthy or diseased brain. --> }}</ref> [[Neurotransmitter receptor|postsynaptic receptors]] for these [[neurotransmitter]]s trigger internal signaling events through a {{abbr|cAMP|cyclic adenosine monophosphate}} pathway and calcium-dependent pathway that ultimately result in increased {{abbr|CREB|cAMP response element-binding protein}} phosphorylation.<ref name="Amphetamine KEGG ΔFosB">{{cite web | title=Amphetamine – Homo sapiens (human) | url=http://www.genome.jp/kegg-bin/show_pathway?hsa05031 | work=KEGG Pathway | accessdate=31 October 2014 | author=Kanehisa Laboratories | date=10 October 2014}}</ref><ref name="Nestler-Renthal Figure 2" /> Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-fos gene with the help of [[corepressor]]s;<ref name="Nestler-Renthal Figure 2">{{cite journal | author = Renthal W, Nestler EJ | title = Chromatin regulation in drug addiction and depression | journal = Dialogues Clin. Neurosci. | volume = 11 | issue = 3 | pages = 257–268 | date = September 2009 | pmid = 19877494 | pmc = 2834246 | doi = | url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834246/figure/DialoguesClinNeurosci-11-257-g002/ | accessdate = 21 July 2014 | quote=}}</ref> c-fos [[gene repression|repression]] acts as a molecular switch that enables the accumulation of ΔFosB in the neuron.<ref name="c-Fos repression">{{cite journal |author=Nestler EJ | title=Review. Transcriptional mechanisms of addiction: role of DeltaFosB | journal = Philos. Trans. R. Soc. Lond., B, Biol. Sci. | volume=363 | issue=1507 | pages=3245–3255 | date=October 2008 | pmid=18640924 | doi=10.1098/rstb.2008.0067 | pmc=2607320 | quote = <!-- Recent evidence has shown that ΔFosB also represses the c-fos gene that helps create the molecular switch—from the induction of several short-lived Fos family proteins after acute drug exposure to the predominant accumulation of ΔFosB after chronic drug exposure—cited earlier (Renthal et al. in press). -->}}</ref> A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for one or two months, slowly accumulates following repeated exposure to stimulants through this process.<ref name="Nestler1" /><ref name="Nestler2">{{cite journal | author = Nestler EJ | title = Transcriptional mechanisms of drug addiction | journal = Clin. Psychopharmacol. Neurosci. | volume = 10 | issue = 3 | pages = 136–143 | date = December 2012 | pmid = 23430970 | pmc = 3569166 | doi = 10.9758/cpn.2012.10.3.136 | quote = The 35-37 kD ΔFosB isoforms accumulate with chronic drug exposure due to their extraordinarily long half-lives.&nbsp;... As a result of its stability, the ΔFosB protein persists in neurons for at least several weeks after cessation of drug exposure.&nbsp;... ΔFosB overexpression in nucleus accumbens induces NFκB}}</ref> ΔFosB functions as "one of the master control proteins" that produces addiction-related [[neuroplasticity|structural changes in the brain]], and upon sufficient accumulation, with the help of its downstream targets (e.g., [[nuclear factor kappa B]]), it induces an addictive state.<ref name="Nestler1">{{cite journal | author = Robison AJ, Nestler EJ | title = Transcriptional and epigenetic mechanisms of addiction | journal = Nat. Rev. Neurosci. | volume = 12 | issue = 11 | pages = 623–637 | date = November 2011 | pmid = 21989194 | pmc = 3272277 | doi = 10.1038/nrn3111 | quote = ΔFosB serves as one of the master control proteins governing this structural plasticity.}}</ref><ref name="Nestler2" />}}}
| caption = {{{caption|This diagram depicts the signaling events in the [[Mesolimbic pathway|brain's reward center]] that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like {{if pagename | Amphetamine = amphetamine| other = [[amphetamine]]}}, {{if pagename| Methylphenidate = methylphenidate| other = [[methylphenidate]]}}, and {{if pagename | Phenethylamine = phenethylamine| other = [[phenethylamine]]}}. Following presynaptic {{if pagename| Dopamine = dopamine| other = [[dopamine]]}} and [[glutamate]] [[cotransmission|co-release]] by such psychostimulants,<ref name="Glutamate-dopamine cotransmission review">{{vcite2 journal | vauthors = Broussard JI | title = Co-transmission of dopamine and glutamate | journal = J. Gen. Physiol. | volume = 139 | issue = 1 | pages = 93–96 | date = January 2012 | pmid = 22200950 | pmc = 3250102 | doi = 10.1085/jgp.201110659 | quote = <!-- Coincident and convergent input often induces plasticity on a postsynaptic neuron. The {{abbr|NAc|nucleus accumbens}} integrates processed information about the environment from basolateral amygdala, hippocampus, and prefrontal cortex (PFC), as well as projections from midbrain dopamine neurons. Previous studies have demonstrated how dopamine modulates this integrative process. For example, high frequency stimulation potentiates hippocampal inputs to the NAc while simultaneously depressing PFC synapses (Goto and Grace, 2005). The converse was also shown to be true; stimulation at PFC potentiates PFC–NAc synapses but depresses hippocampal–NAc synapses. In light of the new functional evidence of midbrain dopamine/glutamate co-transmission (references above), new experiments of NAc function will have to test whether midbrain glutamatergic inputs bias or filter either limbic or cortical inputs to guide goal-directed behavior. -->}}</ref><ref name="Glutamate-dopamine cotransmission review 2">{{vcite2 journal | vauthors = Descarries L, Berube-Carriere N, Riad M, Bo GD, Mendez JA, Trudeau LE | title = Glutamate in dopamine neurons: synaptic versus diffuse transmission | journal = Brain Res. Rev. | volume = 58 | issue = 2 | pages = 290–302 | date = August 2008 | pmid = 18042492 | doi = 10.1016/j.brainresrev.2007.10.005 | quote = <!-- Moreover, all {{abbr|TH|tyrosine hydroxylase}} varicosities which co-localize VGluT2 are synaptic, as if there was a link between the potential of {{abbr|DA|dopamine}} axon terminals to release glutamate and their establishment of synaptic junctions. Together with the RT-PCR and in situ hybridization data demonstrating the co-localization of TH and VGluT2 mRNA in mesencephalic neurons of the {{abbr|VTA|ventral tegmental area}}, these observations raise a number of fundamental questions regarding the functioning of the meso-telencephalic DA system in healthy or diseased brain. --> }}</ref> [[Neurotransmitter receptor|postsynaptic receptors]] for these [[neurotransmitter]]s trigger internal signaling events through a {{abbr|cAMP|cyclic adenosine monophosphate}} pathway and calcium-dependent pathway that ultimately result in increased {{abbr|CREB|cAMP response element-binding protein}} phosphorylation.<ref name="Amphetamine KEGG ΔFosB">{{cite web | title=Amphetamine – Homo sapiens (human) | url=http://www.genome.jp/kegg-bin/show_pathway?hsa05031+2354 | work=KEGG Pathway | accessdate=31 October 2014 | author=Kanehisa Laboratories | date=10 October 2014}}</ref><ref name="Nestler-Renthal Figure 2" /> Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-fos gene with the help of [[corepressor]]s;<ref name="Nestler-Renthal Figure 2">{{cite journal | author = Renthal W, Nestler EJ | title = Chromatin regulation in drug addiction and depression | journal = Dialogues Clin. Neurosci. | volume = 11 | issue = 3 | pages = 257–268 | date = September 2009 | pmid = 19877494 | pmc = 2834246 | doi = | url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834246/figure/DialoguesClinNeurosci-11-257-g002/ | accessdate = 21 July 2014 | quote=}}</ref> c-fos [[gene repression|repression]] acts as a molecular switch that enables the accumulation of ΔFosB in the neuron.<ref name="c-Fos repression">{{cite journal |author=Nestler EJ | title=Review. Transcriptional mechanisms of addiction: role of DeltaFosB | journal = Philos. Trans. R. Soc. Lond., B, Biol. Sci. | volume=363 | issue=1507 | pages=3245–3255 | date=October 2008 | pmid=18640924 | doi=10.1098/rstb.2008.0067 | pmc=2607320 | quote = <!-- Recent evidence has shown that ΔFosB also represses the c-fos gene that helps create the molecular switch—from the induction of several short-lived Fos family proteins after acute drug exposure to the predominant accumulation of ΔFosB after chronic drug exposure—cited earlier (Renthal et al. in press). -->}}</ref> A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for one or two months, slowly accumulates following repeated exposure to stimulants through this process.<ref name="Nestler1" /><ref name="Nestler2">{{cite journal | author = Nestler EJ | title = Transcriptional mechanisms of drug addiction | journal = Clin. Psychopharmacol. Neurosci. | volume = 10 | issue = 3 | pages = 136–143 | date = December 2012 | pmid = 23430970 | pmc = 3569166 | doi = 10.9758/cpn.2012.10.3.136 | quote = The 35-37 kD ΔFosB isoforms accumulate with chronic drug exposure due to their extraordinarily long half-lives.&nbsp;... As a result of its stability, the ΔFosB protein persists in neurons for at least several weeks after cessation of drug exposure.&nbsp;... ΔFosB overexpression in nucleus accumbens induces NFκB}}</ref> ΔFosB functions as "one of the master control proteins" that produces addiction-related [[neuroplasticity|structural changes in the brain]], and upon sufficient accumulation, with the help of its downstream targets (e.g., [[nuclear factor kappa B]]), it induces an addictive state.<ref name="Nestler1">{{cite journal | author = Robison AJ, Nestler EJ | title = Transcriptional and epigenetic mechanisms of addiction | journal = Nat. Rev. Neurosci. | volume = 12 | issue = 11 | pages = 623–637 | date = November 2011 | pmid = 21989194 | pmc = 3272277 | doi = 10.1038/nrn3111 | quote = ΔFosB serves as one of the master control proteins governing this structural plasticity.}}</ref><ref name="Nestler2" />}}}
|header = {{{header|[[Signaling cascade]] in the [[nucleus accumbens]] that results in psychostimulant addiction}}}<br />{{v|t|e|template=Psychostimulant addiction}}
|header = {{{header|[[Signaling cascade]] in the [[nucleus accumbens]] that results in psychostimulant addiction}}}<br />{{v|t|e|template=Psychostimulant addiction}}
|header_align = center
|header_align = center

Revision as of 09:15, 17 April 2015

This annotated image template is intended for transcluding to a variety of psychostimulant and addiction articles, as well as those on related protein topics.
The image file is located at COMMONS:File:ΔFosB.svg and a reusable version of this image is located at COMMONS:File:Annotated ΔFosB.svg screenshot.png.
Signaling cascade in the nucleus accumbens that results in psychostimulant addiction
The image above contains clickable links
This diagram depicts the signaling events in the brain's reward center that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like amphetamine, methylphenidate, and phenethylamine. Following presynaptic dopamine and glutamate co-release by such psychostimulants,[1][2] postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP pathway and calcium-dependent pathway that ultimately result in increased CREB phosphorylation.[3][4] Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-fos gene with the help of corepressors;[4] c-fos repression acts as a molecular switch that enables the accumulation of ΔFosB in the neuron.[5] A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for one or two months, slowly accumulates following repeated exposure to stimulants through this process.[6][7] ΔFosB functions as "one of the master control proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation, with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.[6][7] 
Reflist
  1. ^ Broussard JI (January 2012). "Co-transmission of dopamine and glutamate". J. Gen. Physiol. 139 (1): 93–96. doi:10.1085/jgp.201110659. PMC 3250102. PMID 22200950.
  2. ^ Descarries L, Berube-Carriere N, Riad M, Bo GD, Mendez JA, Trudeau LE (August 2008). "Glutamate in dopamine neurons: synaptic versus diffuse transmission". Brain Res. Rev. 58 (2): 290–302. doi:10.1016/j.brainresrev.2007.10.005. PMID 18042492.
  3. ^ Kanehisa Laboratories (10 October 2014). "Amphetamine – Homo sapiens (human)". KEGG Pathway. Retrieved 31 October 2014.
  4. ^ a b Renthal W, Nestler EJ (September 2009). "Chromatin regulation in drug addiction and depression". Dialogues Clin. Neurosci. 11 (3): 257–268. PMC 2834246. PMID 19877494. Retrieved 21 July 2014.
  5. ^ Nestler EJ (October 2008). "Review. Transcriptional mechanisms of addiction: role of DeltaFosB". Philos. Trans. R. Soc. Lond., B, Biol. Sci. 363 (1507): 3245–3255. doi:10.1098/rstb.2008.0067. PMC 2607320. PMID 18640924.
  6. ^ a b Robison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nat. Rev. Neurosci. 12 (11): 623–637. doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. ΔFosB serves as one of the master control proteins governing this structural plasticity.
  7. ^ a b Nestler EJ (December 2012). "Transcriptional mechanisms of drug addiction". Clin. Psychopharmacol. Neurosci. 10 (3): 136–143. doi:10.9758/cpn.2012.10.3.136. PMC 3569166. PMID 23430970. The 35-37 kD ΔFosB isoforms accumulate with chronic drug exposure due to their extraordinarily long half-lives. ... As a result of its stability, the ΔFosB protein persists in neurons for at least several weeks after cessation of drug exposure. ... ΔFosB overexpression in nucleus accumbens induces NFκB
  1. ^ Template:Multicol
      Ion channel
      G proteins & linked receptors
      (Text color) Transcription factors
    Template:Multicol-end
Retrieved from "https://en.wikipedia.org/w/index.php?title=Template:Psychostimulant_addiction&oldid=656876212"