RGD Reference Report - Short-term cocaine treatment causes neuroadaptive changes in Galphaq and Galpha11 proteins in rats undergoing withdrawal. - Rat Genome Database

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Short-term cocaine treatment causes neuroadaptive changes in Galphaq and Galpha11 proteins in rats undergoing withdrawal.

Authors: Carrasco, GA  Damjanoska, KJ  D'Souza, DN  Zhang, Y  Garcia, F  Battaglia, G  Muma, NA  Van de Kar, LD 
Citation: Carrasco GA, etal., J Pharmacol Exp Ther. 2004 Oct;311(1):349-55. Epub 2004 Jun 2.
RGD ID: 5133684
Pubmed: PMID:15175423   (View Abstract at PubMed)
DOI: DOI:10.1124/jpet.104.069807   (Journal Full-text)

One of the characteristics of drug dependence is that a drug has to be administered repeatedly before withdrawal effects can be observed. We have previously shown that withdrawal after 14 days of cocaine treatment produces a supersensitivity of hypothalamic 5-hydroxytryptamine (serotonin) 2A (5-HT(2A)) receptors, which is accompanied by increases in the levels of Galpha(q) and Galpha(11) proteins. Unfortunately, the exact duration of cocaine treatment necessary to induce alterations in G protein levels during cocaine withdrawal is unknown. The present study investigated the minimum cocaine treatment period required to produce changes in protein levels of membrane- and cytosol-associated Galpha(q) and Galpha(11) proteins in the hypothalamic paraventricular nucleus, amygdala, and frontal cortex. Rats were injected with cocaine (15 mg/kg i.p., b.i.d.) for 0, 1, 3, 5, and 7 days and tested after 2 days of withdrawal. The levels of Galpha(q) and Galpha(11) proteins were increased in the paraventricular nucleus and the amygdala but not in the frontal cortex. Although 1 and 3 days of cocaine treatment were sufficient to maximally elevate the protein levels of Galpha(11) and Galpha(q) proteins in the amygdala, 5 days of treatment were required to maximally increase the levels of Galpha(11) and Galpha(q) proteins in the paraventricular nucleus. The data suggest that the amygdala shows a faster neuroadaptation to the effects of cocaine than the hypothalamic paraventricular nucleus. These findings provide insight into the relative importance of individual components of 5-HT(2A) receptor signal transduction system in regulating the overall sensitivity of this signaling in cocaine-treated rats.

Objects referenced in this article
Gene Gna11 G protein subunit alpha 11 Rattus norvegicus
Gene Gnaq G protein subunit alpha q Rattus norvegicus
Gene Gnaz G protein subunit alpha z Rattus norvegicus

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