al. 1998). Evidence of tolerance to EtOH inhibition during acute exposure has also been observed in hippocampal slices (Grover et al. 1994; Miyakawa et al. 1997). Overall, it appears that NMDAR function is still suppressed during intoxication even after prolonged EtOH exposure, and thus the increase in NMDAR function is likely to be dramatic after EtOH withdrawal following chronic exposure. One consequence of the increase in NMDAR-mediated calcium influx appears to be an increase in susceptibility to excitotoxic effects of NMDA (Chandler et al. 1993; Iorio et al. 1993), although enhanced NMDAR-mediated neuroprotection can also be observed in young cerebellar granule neurons (Pantazis et al. 1998). It has thus been postulated that excitotoxicity during EtOH withdrawal contributes to alcohol-related neuronal loss in the brain.
