Taken together, the evidence from preclinical alcoholism models as well as clinical studies suggests that alcohol alters glial cell density and has profound effects on glutamatergic neurotransmission that may be responsible for neurotoxicity and the modulation of treatment response. Excessive alcohol intake also affects glutamate transporter expression, and vice versa, possibly in an attempt to maintain homeostasis. Furthermore, altered transporter expression/function leads to increased vulnerability for alcohol preference/consumption. Finally, genotypic variations also alter glutamate transporter expression/function and alcohol intake in both rodents and humans.
