Prenatal nicotine exposure increases hyperventilation in α4-knock-out mice during mild asphyxia

Abstract

Prenatal nicotine exposure alters breathing and ventilatory responses to stress through stimulation of nicotine acetylcholine receptors (nAChRs). We tested the hypothesis that α4-containing nAChRs are involved in mediating the effects of prenatal nicotine exposure on ventilatory and metabolic responses to intermittent mild asphyxia (MA). Using open-flow plethysmography, we measured ventilation (V˙E) and rate of O2 consumption (V˙O2) of wild-type (WT) and α4-knock-out (KO) mice, at postnatal (P) days 1-2 and 7-8, with and without prenatal nicotine exposure (6mgkg-1day-1 beginning on embryonic day 14). Mice were exposed to seven 2min cycles of mild asphyxia (10% O2 and 5% CO2), each interspers..