Developmental neurotoxicity impairs ventilatory control: insight from an amphibian model

Abstract

Neurotoxins (nicotine, ethanol) elicit deficits in neuroventilation by impairing responses to CO2. This may explain why these toxins are risk factors for SIDS. We recorded neuroventilation from tadpole hindbrains before and during CO2 stimulation. Recordings were made during acute toxin exposure of hindbrains from naïve animals or following chronic toxin exposure of intact animals. Acute nicotine exposure decreased baseline neuroventilation in some tadpole stages but did not alter CO2 responses. Acute ethanol exposure depressed baseline neuroventilation but did not alter CO2 responses. Chronic exposure (nicotine or ethanol) abolished CO2 responses. These data indicate that chronic and acute toxin exposures differentially impair the neuroventilation. To determine the potential for recovery, tadpoles were returned to control conditions following chronic toxin exposure. Impairment by chronic nicotine disappeared over a 3 wk recovery period, but impairment by chronic ethanol persisted despite 6 wk recovery. Chronic ethanol causes a persistent developmental deficit in the neuroventilatory CO2 response, whereas chronic nicotine produces transient impairment. To determine whether neurogenesis underlies recovery, we exposed recovering tadpoles to BrDU. BrDU labeling unique to nicotine‐recovery animals could indicate regeneration of neurons critical to the CO2 response.