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Serotonin Modulates Ethanol‐Induced Depression in Cerebellar Purkinje Neurons
Author(s) -
Wang Yun,
Jeng ChunHueih,
Lin JiannChyun,
Wang JiaYi
Publication year - 1996
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1996.tb01117.x
Subject(s) - autoreceptor , serotonin , chemistry , agonist , cerebellum , neuroscience , ethanol , long term potentiation , antagonist , 5 ht receptor , electrophysiology , medicine , endocrinology , receptor , biology , biochemistry
In the present study, we found that local application of serotonin (5‐HT) potentiated ethanol‐induced depressions of 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 quantitatively smaller than 5‐HT‐induced potentiation of ethanol depression. Previous reports suggested that the release of 5HT 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, facilited ethanol‐mediated responses. This methiothepin effect was greatly diminished in neonatally 5,7‐dihydroxyhyptamine‐lesioned animals, suggesting a presynaptic mechanism was involved. We also found that the 5‐HT IA antagonist UH301 did not attenuate 5‐HT‐facilitated ethanol reactions. On the other hand, local application of SHT IB agonist CGS12066B potentiated ethanol‐induced depression. Taken together, our data suggest that 5‐HT can modulate ethanol‐mediated electrophysiological depression, possibly mediated through CHT, receptors in the cerebellum.