Juvenile bullfrogs previously identified as highly sensitive to acute nicotine, demonstrated normal neuroventilation following 3 wk of chronic nicotine exposure. Acute bath application of 1 microM galantamine, an acetylcholinesterase inhibitor, significantly attenuated both bullfrog normocapnic neuroventilation and response to hypercapnia in a fashion similar to that of acute nicotine. This would suggest that the developmental increase in nicotine sensitivity does not enhance vulnerability to chronic exposure, and that acute nicotine acts via endogenous acetylcholine pathways to depress neuroventilation and hypercapnic drive.
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