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Darstein M, Albrecht C, Lopez-Francos L, Knorle R, Holter SM, Spanagel R, Feuerstein TJ: Release and accumulation of neurotransmitters in the rat brain: acute effects of ethanol in vitro and effects of long-term voluntary ethanol intake. Alcohol Clin Exp Res. 1998 May;22(3):704-9.
Release from and accumulation in tissue slices of some neurotransmitters under acute ethanol in naive rats and in long-term voluntarily ethanol drinking rats were investigated. Slices of the rat caudatoputamen were prelabeled with [3H] choline and release of [3H] acetylcholine was stimulated through either N-methyl-D-aspartate (NMDA) receptors or strychnine-sensitive glycine receptors. Ethanol in vitro at 2 per thousand, 4 per thousand, and 6 per thousand (34 mM, 68 mM, and 102 mM, respectively) concentration-dependently depressed the maximum effect of the concentration-response curve of NMDA in naive rats. In contrast, voluntary ethanol consumption over months led to a significantly enhanced NMDA receptor response characterized by an increase in the maximum effect of the concentration-response curve. The glycine receptor-mediated release of [3H] acetylcholine, which is inhibited by acute ethanol in a competitive-like fashion, was not changed in animals that ingested ethanol over months. Electrically evoked release of [3H] noradrenaline ([3H] NA) and its presynaptic modulation by morphine through mu-opioid receptors in neocortical slices of the rat, preloaded with [3H] NA, was nearly identical in both ethanol-naive rats and in ethanol drinking rats. The accumulation of [3H] gamma-aminobutyric acid in rat cerebellum tissue was neither affected by acute ethanol in vitro nor after chronic ethanol consumption. In summary, long-term voluntary ethanol intake caused a significant increase in NMDA receptor function in the rat caudatoputamen, but did not result in changes in glycine-evoked [3H] acetylcholine release of electrically evoked [3H] NA release modulated by morphine or cerebellar [3H] gamma-aminobutyric acid accumulation. |
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