Audiogenic seizures in mice whose parents drank alcohol.

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Abstract
The effect of pre- and postnatal exposure to alcohol on susceptibility to audiogenic seizures was studied in C57B1/10 Bg and DBA/Bg mice. For 32 days prior to mating, groups of mice of each strain (12 to 28 females/group, 1 male for every 4 females) were maintained on mouse chow and a 10% (vol/vol) alcohol solution ad lib; nutritional control groups were pair-fed reduced amounts of chow and amounts of 16.2% glucose solution equicaloric to alcohol; normally fed control groups received chow and tap water ad lib. After mating, the females remained on their respective treatments until 14 days post parturition. Compared with the normally fed controls, the alcohol-fed C57 mothers reduced their food consumption by 18% during mating and pregnancy and by 14% after delivery; the DBA mothers, 11 and 3%. At breeding age C57 males consumed about 14 g of alcohol/kg body wt/per day; DBA males, 10 g/kg. Daily intake by C57 and DBA females during breeding and pregnancy was 15 and 13 g/kg; after delivery, 19 and 14; and on day 14 postpartum, 28 and 21. Beginning at 29 days of age groups of offspring (86-158 per group) were tested for audiogenic seizure (90 s of a bell at 95-105 dB) once a day for 4 days, and separate groups at 45 days of age. Of the C57 mice whose parents drank alcohol, 50% had at least 1 seizure, consituting 56% more than both the nutritional and water control groups. Almost all DBA mice had seizures; the offspring of the alcohol-fed parents had significantly more on day 1 than either control group, and more on days 2 and 3 than the water control group. Latency to onset of seizure was 20% shorter in alcohol-fed mice than in nutritional controls and 15% shorter than in the water controls. Alcohol exposure during early development directly caused an increased susceptibility to audiogenic seizures, since the responses of nutritional controls were not different from those of normally fed controls. Alcohol shortened latency to seizure whereas nutritional deficiencies had an effect in the opposite direction. Hyperexcitability of CNS may develop as a result of early exposure to alcohol.