Prenatal SO2 exposure alters brainstem neurons that mediate parasympathetic control of heart rate

Abstract

Human-based studies have concluded that SO2 exposure results in decreased parasympathetic activity (increased resting heart rate and decreased heart rate variability), however the mechanisms responsible for the adverse effects of SO2 are not well understood. The EPA has stated that there is a lack of research focusing on the health effects of prenatal and neonatal SO2 exposure. To address this, an exposure chamber was designed to expose pregnant Sprague-Dawley rats to 5 ppm SO2 for one hour daily during pregnancy and one week after giving birth. In neonatal rats (postnatal days 2–7), premotor cardioinhibitory vagal neurons (CVNs) in the nucleus ambiguus were identified in an in vitro brainstem slice preparation retaining rhythmic respiratory activity. Individual CVNs were whole-cell patch clamped and isolated for either spontaneous glutmatergic neurotransmission or inspiratory-related glycinergic and GABAergic neurotransmission. Preliminary results indicate that inspiratory-related glycinergic and GABAergic neurotransmission to CVNs is unchanged, while glutamatergic neurotransmission to CVNs is significantly diminished. This suggests that a cellular target of SO2 exposure is a decreased excitatory glutamatergic neurotransmission to CVNs, causing decreased parasympathetic control of resting heart rate, autonomic imbalance, and tachycardia. Research funded by GW Institute for Sustainability Research, Education, and Policy Research Award.