Template:Psychostimulant addiction

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This annotated image template is intended for transcluding to a variety of psychostimulant and addiction articles, as well as those on related protein topics.
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Full parameter set: {{Psychostimulant addiction | caption= | header= | headerbg= | align= | Colorcode= }}

Template parameters
Parameter Description Type Default Auto value Status
caption parameter caption This optional parameter may be used to replace the default caption. string See template empty optional
header parameter header This optional parameter may be used to replace the default header. string See template empty optional
header background color headerbg This optional parameter may be used to replace the default header color. string Salmon empty optional
image alignment parameter align This parameter may be set to left, right, or center. string center empty optional
Color legend in a reference Colorcode If set to "no" (i.e., Colorcode=no), the image will not transclude the annotated "Color legend" reference on the image; otherwise, a reference group for "Color legend" must be included on the page where this template is transcluded! string unspecified empty optional

Signaling cascade in the nucleus accumbens that results in psychostimulant addiction

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, phenethylamine, and cocaine. Following presynaptic dopamine and glutamate co-release by such psychostimulants, postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP pathway and calcium-dependent pathway that ultimately result in increased CREB phosphorylation.[1][2] Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-fos gene with the help of corepressors.[2] 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.[3][4] 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.[3][4]
Reflist
  1. ^ Kanehisa Laboratories (10 October 2014). "Amphetamine – Homo sapiens (human)". KEGG Pathway. Retrieved 31 October 2014. 
  2. ^ a b Renthal W, Nestler EJ (2009). "Chromatin regulation in drug addiction and depression". Dialogues Clin. Neurosci. 11 (3): 257–268. PMC 2834246. PMID 19877494. Retrieved 21 July 2014. 
  3. ^ 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. 
  4. ^ 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