Thesis (M.S.) University of Alaska Fairbanks, 2008Developmental exposure to the neuroteratogen nicotine may affect ventilatory responses to hypercapnia. Developmental changes in normocapnic and hypercapnic neuroventilation of the isolated bullfrog brainstem preparation have been previously characterized. I investigated the effect of 3- and 10-wk chronic nicotine (30 [mu]g/L) exposure on lung burst frequency exhibited by early and late metamorphic bullfrog tadpoles during normocapnia (1.5 % CO₂) and hypercapnia (5.0 % CO₂). Chronic nicotine exposure impairs the hypercapnic neuroventilatory response of early metamorphic tadpoles following both 3- and 10-wk exposure. Late metamorphic tadpoles demonstrated an impaired hypercapnic neuroventilatory response only after 10-wk exposure. Chronic nicotine exposure had no effect on normocapnic neuroventilation. Brainstem preparations from early and late metamorphic tadpoles and juvenile bullfrogs were exposed acutely to 18 [mu]g/L nicotine. Acute nicotine had no effect on normocapnic or hypercapnic neuroventilation of early metamorphic tadpoles. Late metamorphic tadpoles and juvenile bullfrogs demonstrated depressed normocapnic neuroventilation in response to acute nicotine exposure, while late metamorphic tadpole brainstems responded significantly to hypercapnia during acute exposure. This suggests that bullfrogs have a differential response to acute nicotine exposure that increases with development. Collectively these data suggest that the consequences of developmental nicotine exposure differ between acute and chronic exposure and throughout bullfrog development.1. Timing and duration of developmental nicotine exposure contribute to attenuation of the tadpole hypercapnic response -- 2. Nicotine affects the normocapnic and hypercapnic neuroventilation of bullfrogs in a developmental stage dependent manner -- General conclusions -- Literature cited
