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Dernière publication 01/12/2008

Chronic voluntary ethanol intake hypersensitizes 5-HT1A autoreceptors in C57BL a

Alcoholism is a complex disorder involving, among others, the serotoninergic (5-HT) system, mainly regulated by 5-HT1A autoreceptors in the dorsal...

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    [title] => Chronic voluntary ethanol intake hypersensitizes 5-HT1A autoreceptors in C57BL a
    [paragraph] => Chronic voluntary ethanol intake hypersensitizes 5-HT1A autoreceptors in C57BL/6J mice.
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Authors
S. Kelaï, T. Renoir, L. Chouchana, F. Saurini, N. Hanoun et al.



 Lab
UPMC Univ Paris 06, UMR-5677, Neuropsychopharmacologie, Paris, France ; INSERM UMR-5677, Neuropsychopharmacologie, Paris, France


Journal
Journal of Neurochemistry


Abstract
Alcoholism is a complex disorder involving, among others, the serotoninergic (5-HT) system, mainly regulated by 5-HT1A autoreceptors in the dorsal raphe nucleus. 5-HT1A 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-HT1A 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-HT1A autoreceptor functional state was assessed using different approaches. Acute administration of the 5-HT1A 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-HT1A autoreceptor-mediated stimulation of [35S]GTP-_-S binding in the dorsal raphe nucleus. These data showed that chronic voluntary ethanol intake in C57BL/6J mice induced 5-HT1A 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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