Current concepts of the mechanisms underlying many of the pharmacological e
ffects of ethanol on the CNS involve disruption of ion channel function via
the interaction of ethanol with specific hydrophobic sites on channel subu
nit proteins. Of particular clinical importance is the development of toler
ance and dependence to ethanol, and it is likely that adaptive changes in s
ynaptic function in response to ethanol's actions on ion channels play a ro
le in this process. In this article, Judson Chandler, Adron Harris and Fult
on Crews discuss potential mechanisms of ethanol-induced changes in synapti
c function that might provide a cellular basis for ethanol tolerance and de
pendence. It is proposed that multiple mechanisms are involved that include
both transcriptional and past-translational modifications in NMDA and GABA
(A) receptors.