Regulation of brain anandamide by acute administration of ethanol
Résumé
The endogenous cannabinoid anandamide participates in the neuroadaptations associated with chronic ethanol exposure. However, no studies describe the acute actions of ethanol on anandamide production and degradation. In the present study we investigated the time-course of the effects of the peripheral administration of ethanol (4 gr/kg, i.p.) on the endogenous levels of anandamide in central and peripheral tissues. Acute ethanol administration decreased anandamide in the cerebellum, the hippocampus and the ventral striatum, as well as in plasma and adipose tissue. Parallel decreases of a second acylethanolamide, palmithylethanolamide were observed in the brain. Effects were observed 45-90 min after ethanol administration. In vivo studies revealed that anandamide decreases were associated with a remarkable inhibition of the release of both anadamide and glutamate release in the ventral striatum. There were no changes in the expression and enzimatic activity of the main enzyme that degradates anandamide, the fatty acid amidohydrolase. Acute ethanol did not change neither the activity of n-acyltransferase, the enzyme that catalyzes the synthesis of the anandamide precursor, nor the expression of NAPE-PLD, the enzyme that releases anandamide from membrane phospholipid precursors. These results suggest that receptor-mediated release of acylethanolamide is inhibited by the acute administration of ethanol, and that this effect is not derived of increased fatty acid ethanolamide degradation.
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