In the present study, we found that local application of serotonin (5- HT) potentiated ethanol-induced depressions at the spontaneous activity of Purkinje neurons in urethane-anesthetized rats. 5-HT also potentiated depressions induced by γ-aminobutyric acid; however, this modulatory response was qualitatively smaller than 5-HT-induced potentiation of ethanol depression. Previous reports suggested that the release of 5-HT can be regulated by presynaptic 5-HT autoreceptors. We found that local application of methiothepin, which may induce 5-HT overflow through the inhibition of presynaptic autoreceptors, facilitated ethanol-mediated responses. This methiothepin effect was greatly diminished in neonatally 5,7- dihydroxytryptamine-lesioned animals, suggesting a presynaptic mechanism was involved. We also found that the 5-HT(1A) antagonist UH301 did not attenuate 5-HT-facilitated ethanol reactions. On the other hand, local application of 5-HT(1B) agonist CGS12066B potentiated ethanol-induced depression. Taken together, our data suggest that 5-HT can modulate ethanol-mediated electrophysiological depression, possibly mediated through 5-HT(1B) receptors in the cerebellum.
|Number of pages||8|
|Journal||Alcoholism: Clinical and Experimental Research|
|Publication status||Published - 1996|
- Purkinje Neurons
ASJC Scopus subject areas
- Psychiatry and Mental health
- Medicine (miscellaneous)