Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Acute abuse of alcohol is well known to have deleterious effects on memory. However, the molecular and cellular bases of this effect are not well understood. Ethanol is known to inhibit long-term potentiation (LTP), a putative cellular substrate of memory. However, there is controversy concerning the doses of ethanol required for inhibition of LTP. We examined the doses of ethanol required to inhibit LTP in the CA1 region of the hippocampus. We used two different LTP-inducing paradigms in these studies and found that only doses of ethanol associated with profound intoxication (50-100 mM) can produce significant inhibition of LTP. We also investigated the molecular mechanisms of ethanol's effect on LTP. Activation of the N-methyl-D-aspartate receptor plays a critical role in LTP, and ethanol has been shown to partially inhibit N-methyl-D-aspartate receptor function. We tested directly whether the level of N-methyl-D-aspartate inhibition produced by 100 mM ethanol is sufficient to account for the complete inhibition of LTP produced by 100 mM ethanol. Our data suggest that ethanol's effects on the N-methyl-D-aspartate receptor can account for most, but not all of ethanol's inhibition of LTP.

Original publication




Journal article


Alcohol Clin Exp Res

Publication Date





404 - 408


Alcoholic Intoxication, Animals, Culture Techniques, Dose-Response Relationship, Drug, Ethanol, Hippocampus, Long-Term Potentiation, Male, Rats, Rats, Sprague-Dawley, Receptors, N-Methyl-D-Aspartate