Chronic alcohol intake is associated with widespread disruptions in sleep and circadian rhythms in both human alcoholics and in experimental animals. Recent studies have demonstrated that chronic and acute ethanol treatments alter fundamental properties of the circadian pacemaker—including free-running period and responsiveness to photic and nonphotic phase-shifting stimuli—in rats and hamsters. In the present work, the authors extend these observations to the C57BL/6J mouse, an inbred strain characterized by very high levels of voluntary ethanol intake and by reliable and stable free-running circadian activity rhythms. Mice were housed individually in running-wheel cages under conditions of either voluntary or forced ethanol intake, whereas controls were maintained on plain water. Forced ethanol intake significantly attenuated photic phase delays (but not phase advances) and shortened free-running period in constant darkness, but voluntary ethanol intake failed to affect either of these parameters. Thus, high levels of chronic ethanol intake, beyond those normally achieved under voluntary drinking conditions, are required to alter fundamental circadian pacemaker properties in C57BL/6J mice. These observations may be related to the relative ethanol insensitivity displayed by this strain in several other phenotypic domains, including ethanol-induced sedation, ataxia, and withdrawal. Additional experiments will investigate chronobiological sensitivity to ethanol in a range of inbred strains showing diverse ethanol-related phenotypes.

Background and ObjectiveAnimal studies can be a great tool to investigate sex differences in a variety of different ways, including behavioral and physiological responses to drug treatments and different “lifestyle variables” such as diets. Consumption of both high‐fat diets and alcohol is known to affect anxiety behaviors and overall health. This project investigated how high‐fat diet and alcohol access and its combination affected the behavior and physiology of male and female C57BL/6J mice.MethodMice were separated into three food groups: high‐fat diet, 10% fat diet, and regular chow, and each group was paired with either water or 10% alcohol. Behavioral assays included diet and alcohol preference, light‐dark box, open field, and feeding and drinking measurements. Physiological measures included glucose tolerance tests and measurement of brain‐derived neurotrophic factor, insulin, and leptin levels.ResultsFemales and males differed in the open field, as male mice decreased activity, while females increased activity when consuming high‐fat diet. While females consumed more ethanol than males, alcohol consumption was able to improve glucose tolerance and increase anxiety in both sexes. Lastly, females were more resistant to the physiological changes caused by high‐fat diet than males, as females consuming high‐fat diet exhibited decreased insulin secretion, less change to brain‐derived neurotrophic factor levels, and better glucose tolerance than males consuming high‐fat diet.ConclusionThese results suggest that the response to high‐fat diet and alcohol consumption is sex dependent and that males are more affected both behaviorally and physiologically by high‐fat diet compared to females.

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.

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