RGD Reference Report - Dopamine receptor mechanisms mediate corticotropin-releasing factor-induced long-term potentiation in the rat amygdala following cocaine withdrawal. - Rat Genome Database

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Dopamine receptor mechanisms mediate corticotropin-releasing factor-induced long-term potentiation in the rat amygdala following cocaine withdrawal.

Authors: Krishnan, B  Centeno, M  Pollandt, S  Fu, Y  Genzer, K  Liu, J  Gallagher, JP  Shinnick-Gallagher, P 
Citation: Krishnan B, etal., Eur J Neurosci. 2010 Mar;31(6):1027-42. Epub 2010 Mar 8.
RGD ID: 6907453
Pubmed: PMID:20377617   (View Abstract at PubMed)
PMCID: PMC3118420   (View Article at PubMed Central)
DOI: DOI:10.1111/j.1460-9568.2010.07148.x   (Journal Full-text)

Corticotropin-releasing factor (CRF) in the amygdala is involved in stress responses. Moreover, dopaminergic neurotransmission in the brain reward system including the amygdala plays a significant role in the pathology of cocaine addiction. The present study analysed CRF-induced synaptic plasticity, its pharmacological sensitivity and interactions with the dopamine (DA) system in the basolateral to lateral capsula central amygdala (lcCeA) pathway after a 2-week withdrawal from repeated cocaine administration. A physiologically relevant CRF concentration (25 nm) induced long-term potentiation (LTP) that was enhanced after cocaine withdrawal. In saline-treated rats, CRF-induced LTP was mediated through N-methyl-d-aspartate (NMDA) receptors, L-type voltage-gated calcium channels (L-VGCCs) and CRF(1) receptors. However, in cocaine-withdrawn animals, activation of CRF(1) and CRF(2) receptors was found to enhance LTP. This enhanced CRF-induced LTP after cocaine withdrawal was mediated through endogenous activation of both D1- and D2-like receptors. Furthermore, expression of the D1 receptor (D1R) but not the D2R, D3R, D4R or D5R was significantly increased after cocaine withdrawal. CRF(1) but not CRF(2) protein expression was increased, suggesting that elevated levels of these proteins contributed to the enhancement of CRF-induced LTP during cocaine withdrawal. CRF interactions with the DA system in the amygdala may represent a fundamental neurochemical and cellular mechanism linking stress to cocaine-induced neuronal plasticity.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
positive regulation of long-term synaptic potentiation  IMP 6907453; 6907453 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Drd1  (dopamine receptor D1)
Drd2  (dopamine receptor D2)


Additional Information