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Updated: Jul 5, 2026

Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder
Published on: June 23, 2023
Acute and chronic ethanol exposure differentially affect induction of hippocampal LTP
Satoshi Fujii1, Yoshihiko Yamazaki, Toshimichi Sugihara
1Department of Physiology, Yamagata University School of Medicine, Yamagata 990-9585, Japan. sfujii@med.id.yamagata-u.ac.jp
Abstract:
Using hippocampal slices, we found that chronic ethanol consumption by rats induces tolerance to the impairing effects of acute ethanol treatment on induction of long-term potentiation (LTP) in CA1 neurons. In hippocampal slices from pair-fed control rats, stable LTP was induced by tetanic stimulation consisting of 25 or more pulses at 100 Hz, but not by tetanic stimulation of 15 pulses at 100 Hz, and LTP induction was blocked if the tetanus was delivered in the presence of 8.6 mM ethanol, 1 microM muscimol, a gamma-aminobutyric acid (GABA) A receptor agonist, or 2.5 microM dl-2-amino-5-phosphonovaleric acid (AP5), an N-methyl-d-aspartate (NMDA) receptor antagonist. In hippocampal slices from rats chronically fed a liquid diet containing ethanol, a tetanus consisting of 15 pulses at 100 Hz did induce stable LTP, indicating a decrease in the stimulation threshold for inducing LTP. Application of ethanol, muscimol, or AP5 did not affect LTP induction in these cells, suggesting that the effects of chronic ethanol exposure on LTP induction are mediated by a reduction in GABAergic inhibition or an increase in NMDA receptor activity in hippocampal CA1 neurons.
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