DEVELOPMENTAL THERMOREGULATORY DEFICITS IN PRENATAL ETHANOL EXPOSED LONG-SLEEP AND SHORT-SLEEP MICE

Sensitivity to alcohol may influence the severity of prenatal alcohol effects. To examine this hypothesis, the ontogeny of thermoregulation was measured in prenatal ethanol exposed offspring of mice selected for differences in alcohol sensitivity. Pregnant long-sleep (LS) and short-sleep (SS) mice were exposed to 3 or 4 g/kg ethanol or an isocaloric amount of maltose-dextrin twice per day from day 7 through 18 of pregnancy. Doses were given six hours apart via gavage. Nonintubated lab chow controls were included for both genotypes. Offspring were fostered at birth to lactating mice of an outbred strain. Offspring temperatures were measured at 0, 60, and 120 min away from the nest on alternating days from 7 through 21 days of age. LS and SS offspring prenatally exposed to the high ethanol dose showed lower temperatures at the 60 and 120 min time points on each day of testing compared to all other treatment groups. Temperatures of offspring prenatally exposed to the low ethanol dose did not differ from controls. These results suggest a relatively steep dose-response curve for thermoregulatory deficits in LS and SS offspring prenatally exposed to alcohol. Genetically-based alcohol sensitivity did not influence the effects of prenatal alcohol exposure on this response.