Chronic and acute ethanol exposures differentially impair neuroventilation in developing bullfrogs

Abstract

Acute and chronic developmental exposures to ethanol are associated with neurological and ventilatory impairments; however, the neuroventilatory impairments have been less studied. Neuroventilation of the tadpole brainstem has been well characterized and is an excellent model for assessing neuroventilatory impairments that may result from teratogen exposure. We recorded neural correlates of breathing from tadpole brainstems challenged with hypercapnia during acute bath application of ethanol and after chronic exposure of the intact animals for 10 wk. Brainstems from early‐development (ED) and late‐development (LD) tadpoles decreased lung bursting following acute ethanol exposure, but appropriately responded to hypercapnic challenges with increases in lung bursting. Brainstems from ED and LD tadpoles chronically exposed to ethanol failed to respond to hypercapnia, but exhibited no reduction in lung bursting prior to hypercapnic challenge. These data indicate that chronic and acute ethanol exposures differentially impair neuroventilation in the developing bullfrog perhaps suggesting that chronic and acute ethanol exposures exert their deleterious influences via different mechanisms. These mechanisms remain to be identified. NIH 2U54NS041069‐06AI