Abstract

Background: 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/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: [3,H]L-glutamate transport activity (Vmax,) was 699 pmol S min-1, S mg-1, in alcohol-naive cAA rats and 487 pmol S min-1, S mg-1, in alcohol-preferring cAA rats. The specific binding sites (Bmax,) for [3,H]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.

Keywords: alcohol-preferring rats, binding, uptake, glutamate transporter, Glutamate