Joanna Peris, Kevin J. Anderson, Thomas W. Vickroy , Michael. A. King, Bruce E. Hunter and Don W. Walker

7. SUMMARY

LTP has been considered a significant physiological model of memory formation. In light of converging evidence of a critical role for the hippocampus in the formation of memory, LTP may be more than a model of memory. LTP may actually be a significant mechanism utilized by the hippocampus for encoding or indexing experiential representations of activity originating in cortical association areas (114, 115). Chronic alcohol abuse disrupts long-term memory formation in a manner that has not been adequately linked to gross neuropathological abnormalities. CET produces significant changes in the structural and functional properties of the hippocampus in rodents including a profound reduction in LTP at synapses in CA1. In addition to the NMDA receptor/ion channel complex, both GABA and acetylcholine receptors appear especially sensitive to the acute and chronic actions of ethanol. When coupled with the growing recognition of the role of the hippocampus and LTP in normal memory formation; collectively, this evidence provides a compelling rationale for studying CET and LTP. A complete understanding of how CET affects LTP in a persistent fashion will more than likely require an understanding of the probable interactions of these three neurotransmitter systems in hippocampus. A similar "multi-transmitter" approach has recently been successfully applied to the understanding of ethanol tolerance and the mechanism by which repeated exposure to ethanol may affect multiple receptor classes via changes in protein kinase C synthesis and activity (see 116). Thus, the mechanisms underlying the effect of CET on LTP may very likely be a result of changes in a number of neurotransmitter systems in hippocampus including GABAergic, glutamatergic and cholinergic. Even though CET may induce a number of changes in NMDA, GABA and cholinergic receptor number and function in hippocampus, we do not know whether these changes are the mechanism by which CET decreases LTP or to what extent these changes can account for CET effects on LTP. Thus, it is imperative that we test the relationship of the functional status of receptors affected by CET and the induction, maintenance and expression of LTP in CET rats.