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Long Term Effect of Ethanol on GABA-Benzodiazepine Receptors | 43930

International Journal of Pharmacy Teaching & Practices

ISSN - 1986-8111

Abstract

Long Term Effect of Ethanol on GABA-Benzodiazepine Receptors of Rat Brain Regions

Manoochehr Messripour, Azadeh mesripour

Objective: The aim of this study is to investigate the effects of chronic exposure of ethanol ingestion on GABA benzodiazepine receptor complex in four rat brain regions.
Methods: Male adult rats from a colony were house with food and drinking water / ethanol (85%+15% v/v). After 13 months of chronic ethanol consumption, the rats were killed by decapitation and the brain regions dissected and the crude synaptosomal fraction (P2) was prepared in ice-cold 0.32 M sucrose. The resulting pellet was resuspended in Tris-HCl buffer (pH 7.4). The samples were kept frozen at-20 °C until binding determination.
Results: Long term ethanol ingestion by the rat resulted in a decrease Kd values in the strlatum and hippocampus, and an increase of Kd values in the cerebellum and frontal cortex . Long term ethanol consumption had no statistically significant effect on GABA-benzodiazepine binding (B max), but a trend toward a reduction in the all brain regions studied. The different responses of GABA receptor affinity of the brain regions to chronic ethanol ingestion may result from quantitative differences in the distribution of GABA-ergic neurons in the tested brain areas.
Conclusion: The increase in the affinity of the striatum and hippocampus and the decreased affinity of cerebellum and frontal cortex, by long term continues ethanol ingestion, may result from quantitative differences in the Objective: The aim of this study is to investigate the effects of chronic exposure of ethanol ingestion on GABA benzodiazepine receptor complex in four rat brain regions.
Methods: Male adult rats from a colony were house with food and drinking water / ethanol (85%+15% v/v). After 13 months of chronic ethanol consumption, the rats were killed by decapitation and the brain regions dissected and the crude synaptosomal fraction (P2) was prepared in ice-cold 0.32 M sucrose. The resulting pellet was resuspended in Tris-HCl buffer (pH 7.4). The samples were kept frozen at-20 °C until binding determination.
Results: Long term ethanol ingestion by the rat resulted in a decrease Kd values in the strlatum and hippocampus, and an increase of Kd values in the cerebellum and frontal cortex . Long term ethanol consumption had no statistically significant effect on GABA-benzodiazepine binding (B max), but a trend toward a reduction in the all brain regions studied. The different responses of GABA receptor affinity of the brain regions to chronic ethanol ingestion may result from quantitative differences in the distribution of GABA-ergic neurons in the tested brain areas.
Conclusion: The increase in the affinity of the striatum and hippocampus and the decreased affinity of cerebellum and frontal cortex, by long term continues ethanol ingestion, may result from quantitative differences in the distribution of GABA-ergic neurons in the tested brain regions

 
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