Chronic ethanol exposure disrupts neuroventilation and responses to hypoxia in bullfrog tadpoles

Abstract

Chronic early developmental ethanol (EtOH) exposure is a sudden infant death syndrome risk factor and impairs neonatal rat hypoxic ventilatory responses. 10‐wk EtOH exposure impairs tadpole CO2 ventilatory responses. We hypothesized that tadpole hypoxic ventilatory responses would be impaired by EtOH. Neurocorrelates of lung and gill ventilation were recorded from in vitro brainstems of control and 10‐wk EtOH‐exposed tadpoles during normoxia and hypoxia. The tadpole central hypoxic ventilatory response was a reduced lung burst frequency and an increased lung burst duration, and these responses became more pronounced over development. Early‐stage tadpoles also increased gill burst amplitude late in hypoxia. 10‐wk EtOH exposure depressed baseline lung burst frequency and the hypoxia‐induced changes in lung burst duration and gill burst amplitude. Across development, chronic EtOH destabilized neuroventilation. The more marked impairments in late‐stage tadpoles suggest developmentally increased EtOH sensitivity or a disrupted maturation of the hypoxic ventilatory response. Thus, the ventilatory consequences of developmental EtOH exposure are an impaired hypoxic and hypercapnic responses.