Abstract
The effects of ethanol on K +-stimulated and spontaneous release of gamma-aminobutyric acid (GABA) were studied in cortical and cerebellar brain slices obtained from long-sleep (LS) and short-sleep (SS) mice. A superfusion technique was used. Tissue slices were perfused with ethanol (0–515 mM) for 20 min. Ethanol inhibited K +-stimulated 3H-GABA release at lower concentrations in LS cortical slices than in SS slices. Little or no inhibition of K +-stimulated 3H-GABA release was seen in both LS and SS cerebellar slices. The spontaneous release of 3H-GABA was inhibited to equal degrees in LS and SS cerebellar slices but was unaffected in cortical slices, at the concentrations used. The possibility that ethanol inhibits 3H-GABA release by stimulating prostaglandin production was partially tested by assessing the effects of prostaglandin F 2α (PGF 2α) on 3H-GABA release in cortical and cerebellar slices. No effect of PGF 2α on 3H-GABA release was seen in either brain region. These results support the notion that ethanol may elicit some of its actions by inhibiting neurotransmitter release. This effect appears to be influenced by genotype and brain region.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
