to cognitive impairment produced by EtOH. At present, the postsynaptic EtOH effects on neurotransmitter receptors appear to occur within the receptor molecules themselves, although more work is needed to elucidate the roles of post-translation modification. On the presynaptic side, acute EtOH generally potentiates GABA release, contributing to the enhanced neuronal inhibition produced by the drug. The molecular mechanisms involved in EtOH potentiation of GABA release remain to be fully explored. EtOH also alters other aspects of synaptic transmission involving amino acid transmitters and monoamines. The net result of the EtOH effects of transmission seems to be to dampen synaptic excitation in many brain regions and reduce most forms of synaptic plasticity (with noted exceptions).
