Chronic ethanol intake modulates photic and non-photic circadian phase responses in the Syrian hamster.

Chronic alcohol intake disrupts sleep and other circadian biological rhythms in both human alcoholics and in experimental animals. Recent studies from our laboratory indicate that these effects may be due, in part, to ethanol-induced alterations in fundamental properties of the circadian pacemaker. The present study explored the effects of chronic voluntary ethanol intake (25% v/v) on circadian phase responses to both photic and non-photic stimuli in Syrian hamsters. Hamsters were used in these experiments because they are a popular model organism in behavioral chronobiology research, and are characterized by unusually high levels of voluntary ethanol intake. Relative to controls, ethanol-exposed animals showed attenuation of circadian phase responses and wheel running activity following acute administration of the benzodiazepine, triazolam, a non-photic phase-shifting stimulus. In addition, ethanol-exposed animals displayed reduced phase advances, but normal phase delays, in response to brief light pulses. While the mechanisms underlying these effects remain to be elucidated, we hypothesize that ionotropic GABA and glutamate receptors may be involved, since these proteins serve as important targets for the neurobiological effects of ethanol, and are also known to be critically involved in the modulation of photic and non-photic circadian phase responses.