Reprints
PubMed
CAVEAT LECTOR
NEUROCHEMICAL BASIS OF DISRUPTION OF HIPPOCAMPAL LONG TERM POTENTIATION BY CHRONIC ALCOHOL EXPOSURE
Joanna Peris, Kevin J. Anderson, Thomas W. Vickroy , Michael. A. King, Bruce E. Hunter and Don W. Walker
Depts. of Pharmacodynamics , Neuroscience and Physiological Sciences , Center for Alcohol Research , University of Florida Brain Institute , and Gainesville Veteran’s Administration Medical Center
Received 5/29/97; Accepted 6/11/97
1. ABSTRACT
The aim of this review is to summarize the possible mechanisms underlying the long-term impairment of learning and memory resulting from chronic ethanol treatment (CET) especially that involving decrements in long-term potentiation (LTP) in hippocampus. CET for a 28-week duration affects the rat hippocampal formation in such a way as to decrease the magnitude of LTP; an effect that can last as long as 7 months after ethanol withdrawal. It appears that NMDA receptor number in hippocampus is unchanged after CET whereas the data suggest a more pronounced role for changes in GABAergic and cholinergic synaptic transmission in determining how CET influences the induction of LTP in hippocampus. In particular, changes in presynaptic modulation of neurotransmitter release in hippocampus may be one mechanism by which CET inhibits LTP. Thus, the mechanisms underlying the effect of CET on LTP are a result of changes in a number of neurotransmitter systems in hippocampus (GABAergic and cholinergic) rather than based solely on changes in glutamate transmission.