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Glutamate transport is downregulated in the cerebral cortex of alcohol-preferring rats.

INTRODUCTION
Ethanol (EtOH) affects glutamatergic neurotransmission and this may underlie craving in alcoholics. The present study aimed to further elucidate the EtOH-induced modulation of glutamatergic neurotransmission in a model for alcoholism: the alcohol-preferring cAA rat.


MATERIAL AND METHODS
Glutamate transporter binding and function was assessed in membrane and synaptosomal preparations from the cerebral cortex of alcohol-preferring cAA rats and alcohol-naive cAA rats.


RESULTS
[3H]L-glutamate transport activity (Vmax) was 699 pmol.min-1.mg-1 in alcohol-naive cAA rats and 487 pmol.min-1.mg-1 in alcohol-preferring cAA rats. The specific binding sites (Bmax) for [3H]D-aspartate were markedly decreased in alcohol-preferring cAA rats (2059 pmol/mg) as compared to alcohol-naive cAA rats (4275 pmol/mg).


CONCLUSIONS
We hypothesize that the reduced density and function of glutamate transporter sites in alcohol-preferring cAA rats may represent an adaptive mechanism in order to counteract suppressed glutamatergic neurotransmission during chronic EtOH exposure.