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

Carrasco G.A., Damjanoska K.J., D'Souza D.N., Zhang Y., Garcia F., Battaglia G., Muma N.A., Van de Kar L.D.

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.

J. Pharmacol. Exp. Ther. 311:349-355(2004) [PubMed] [Europe PMC]

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