Abstract

Chronic ethanol inhalation produced no change in the number or affinity of [(3)H]flunitrazepam binding sites on well-washed synaptic membranes prepared from male Quackenbush mice, but produced a significant decrease in the capacity of GABA to enhance [(3)H]flunitrazepam binding. This decrease was characterised by a higher EC(50) (1.4 ? M compared to 0.6 ? M) and a lower maximal level of enhancement (162% compared to 172%) for tissue from the chronically treated animals compared to tissue from control animals. Acute ethanol treatment or ethanol incubated in vitro with the brain membranes did not produce changes in any of the [(3)H]flunitrazepam binding parameters. These results support other findings that chronic ethanol may affect the coupling of various sites on GABA-A receptor-ionophore complexes in brain.

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