Template:Psychostimulant addiction

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This annotated image insertion 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.
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TemplateData[edit]

This is the TemplateData documentation for this template used by VisualEditor and other tools.

TemplateData for Psychostimulant addiction

Full parameter set: {{Psychostimulant addiction | caption= | header= | headerbg= | align= | Colorcode= }}

Template parameters

Parameter Description Type Status
caption parameter caption

This optional parameter may be used to replace the default caption.

Default
See template
Example
empty
Auto value
empty
String optional
header parameter header

This optional parameter may be used to replace the default header.

Default
See template
Example
empty
Auto value
empty
String optional
header background color headerbg

This optional parameter may be used to replace the default header color.

Default
Salmon
Example
empty
Auto value
empty
String optional
image alignment parameter align

This parameter may be set to left, right, or center.

Default
center
Example
empty
Auto value
empty
String 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!

Default
unspecified
Example
empty
Auto value
empty
String optional

Signaling cascade in the nucleus accumbens that results in psychostimulant addiction
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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, methamphetamine, 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][5] 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.[6] A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for one or two months, slowly accumulates following repeated high-dose exposure to stimulants through this process.[7][8] 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.[7][8]
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 3250102free to read. 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 2834246free to read. PMID 19877494. Retrieved 21 July 2014. 
  5. ^ Cadet JL, Brannock C, Jayanthi S, Krasnova IN (2015). "Transcriptional and epigenetic substrates of methamphetamine addiction and withdrawal: evidence from a long-access self-administration model in the rat". Mol. Neurobiol. 51 (2): 696–717. doi:10.1007/s12035-014-8776-8. PMC 4359351free to read. PMID 24939695. Figure 1 
  6. ^ 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 2607320free to read. PMID 18640924. 
  7. ^ 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 3272277free to read. PMID 21989194. ΔFosB serves as one of the master control proteins governing this structural plasticity. 
  8. ^ 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 3569166free to read. 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