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  • Title: Chronic voluntary ethanol intake hypersensitizes 5-HT(1A) autoreceptors in C57BL/6J mice.
    Author: Kelaï S, Renoir T, Chouchana L, Saurini F, Hanoun N, Hamon M, Lanfumey L.
    Journal: J Neurochem; 2008 Dec; 107(6):1660-70. PubMed ID: 19094059.
    Abstract:
    Alcoholism is a complex disorder involving, among others, the serotoninergic (5-HT) system, mainly regulated by 5-HT(1A) autoreceptors in the dorsal raphe nucleus. 5-HT(1A) autoreceptor desensitization induced by chronic 5-HT reuptake inactivation has been associated with a decrease in ethanol intake in mice. We investigated here whether, conversely, chronic ethanol intake could induce 5-HT(1A) autoreceptor supersensitivity, thereby contributing to the maintenance of high ethanol consumption. C57BL/6J mice were subjected to a progressive ethanol intake procedure in a free-choice paradigm (3-10% ethanol versus tap water; 21 days) and 5-HT(1A) autoreceptor functional state was assessed using different approaches. Acute administration of the 5-HT(1A) receptor agonist ipsapirone decreased the rate of tryptophan hydroxylation in striatum, and this effect was significantly larger (+75%) in mice that drank ethanol than in those drinking water. Furthermore, ethanol intake produced both an increased potency (+45%) of ipsapirone to inhibit the firing of 5-HT neurons, and a raise (+35%) in 5-HT(1A) autoreceptor-mediated stimulation of [(35)S]GTP-gamma-S binding in the dorsal raphe nucleus. These data showed that chronic voluntary ethanol intake in C57BL/6J mice induced 5-HT(1A) autoreceptor supersensitivity, at the origin of a 5-HT neurotransmission deficit, which might be causally related to the addictive effects of ethanol intake.
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