In this review we have focused on acute and chronic EtOH actions on synaptic transmission. It is not possible to cover all aspects of this topic, and thus we have focused on describing the best established EtOH actions. As the review attests, EtOH affects numerous aspects of synaptic transmission both directly and indirectly, to alter brain function and behavior. Acute exposure to EtOH generally increases the function of cys-loop ligand-gated ion channels, with prominent effects of GABAA and glycine receptors. These actions increase synaptic and extra-synaptic inhibition and are thought to contribute to sedation and other aspects of intoxication. Ionotropic glutamate and P2X receptors are generally inhibited by acute EtOH exposure, with some noted exceptions. The inhibitory effect on ionotropic glutamate receptors is most prominent at NMDARs and on NMDAR-mediated synaptic responses, and this inhibitory action is thought to contribute 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
