Abstract
The amnesic effects of acute ingestion of ethanol are well documented in both human and animal studies (Goodwin et al, 1969; Lowy, 1970; Lister et al., 1987; Zimmerberg et al., 1991; Ryback 1971; Castellano and Populin, 1990; Tako et al., 1991). However, the molecular and cellular mechanisms that underlie these effects are unknown. In the past, the vast majority of studies of learning and memory have been conducted under conditions where it was very difficult to perform cellular and molecular analyses—namely in studies of animal behavior. There are, of course, good reasons to begin studying learning and memory under such complex circumstances, perhaps the most obvious being the limitations of simple systems models of memory. Nonetheless, within the last 25 years, there have been a number of important discoveries which indicate that future research may provide extremely important new information about the cellular and molecular substrates of learning and memory deficits. The discovery of long-term potentiation (LTP) provided a cellular mechanism that had many properties thought to be essential for a biological substrate of memorial processes. Subsequent work revealed that both chronic and acute ethanol inhibited this form of neuronal plasticity (Durand and Carlen, 1984; Sinclair and Lo, 1986; Mulkeen et al, 1987; Blitzer et al., 1990).
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Browning, M., Schummers, J., Bentz, S. (1999). Alcohol, Memory, and Molecules. In: Liu, Y., Hunt, W.A. (eds) The “Drunken” Synapse. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4739-6_12
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DOI: https://doi.org/10.1007/978-1-4615-4739-6_12
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