Developmental exposure to ethanol or nicotine inhibits the hypercapnic ventilatory response in tadpoles.

Tadpoles, Lithobates (formerly Rana) catesbeiana, were held for 8-12 weeks in pond water that was either teratogen free or contained 0.15% ethanol or 30 microg/L nicotine. The ventilatory and neuroventilatory consequences of these developmental exposures were assessed. Developmental exposure to ethanol or nicotine blocked the hypercapnia-induced increase in surfacing frequency typically exhibited by tadpoles, as well as the hypercapnia-induced increase in putative lung ventilation exhibited by isolated tadpole brainstems. It was specifically the hypercapnic ventilatory response, previously characterized as an increase in lung activity, that was affected by developmental exposure to these teratogens. Developmental exposure to ethanol or nicotine did not affect the frequency of surfacing or putative lung breaths exhibited by the intact tadpoles or their isolated brainstems when not subjected to a hypercapnic challenge.