Prenatal ethanol exposure alters development of heart ornithine decarboxylase response to insulin in rat. II. Daily dose.
Timed pregnant rats received daily a bolus of ethanol (4 g/kg, via stomach tube) from the 13th day of gestation and the development of cardiac sympathetic nerve function was determined in the offspring. Stimulation in sympathetic nerve activity was determined by an increase in heart ornithine decarboxylase (ODC) activity evoked by insulin-induced hypoglycemia. In controls, insulin-induced stimulation in heart ODC activity was maximal between 4 and 8 days of postnatal age. However, chlorisondamine pre-treatment decreased this stimulation starting from 6 days of age indicating that the induction in activity from this age is mediated via central stimulation of sympathetic nerves. In contrast, pups whose mothers received ethanol both during gestation and post-partum showed a decreased cardiac ODC response to insulin between 6 and 13 days of age. Withdrawal from ethanol at birth appeared to slow the development of neuronal reflex response to 8 days of age. Prenatal exposure to ethanol also altered the development of brain ODC response to insulin. In both heart and brain, basal ODC activity was increased after ethanol exposure. These data demonstrate that maternal exposure to ethanol even transiently produces alterations in the development of brain and cardiac sympathetic response to insulin in the offspring.
D000818:Animals; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000196:embryology*; D000431:Ethanol / Q000008:administration & dosage / Q000633:toxicity*; D005260:Female; D006321:Heart / Q000196:embryology* / Q000294:innervation; D007328:Insulin / Q000494:pharmacology*; D009206:Myocardium / Q000201:enzymology; D009929:Organ Size / Q000187:drug effects; D009955:Ornithine Decarboxylase / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D013564:Sympathetic Nervous System / Q000196:embryology
D007328:Insulin; D000431:Ethanol; D009955:Ornithine Decarboxylase