The Effects of Developmental Nicotine Exposure on Hypoglossal Motoneuron Primary Dendrite and Soma Development in the Neonatal Rat

Abstract

Nicotine from smoking or from other products containing nicotine has adverse effects on the fetus during pregnancy, such as respiratory problems. Our laboratory has previously shown that exposure to nicotine during development (DNE) alters hypoglossal motor neuron (XII MN) function, including decreased excitatory synaptic input, desensitized nicotinic acetylcholine receptors, increased input resistance, and differences in the precision and reliability of spike timing in XIIMNs. Evidence of DNE effects on XIIMN function prompted us to test the hypothesis that DNE will affect the development of primary dendrites and the soma. Brainstem slices were collected from neonates and motoneurons were filled with neurobiotin via whole-cell patch clamp. Filled cells were visualized with heavy metal intensified-3,3'-Diaminobenzidine (DAB) reaction. DAB-stained cells were analyzed using Neurolucida hardware and software. On average, the maximum soma diameter of more rostral XIIMNs was larger than that in more caudal cells. Also, caudal XIIMNs had more primary nodes than rostral XIIMNs, and there was a significant treatment effect on minimum soma diameter (Control, 13.76 ± 0.71 µm; DNE, 18.09 ± 1.22 µm). The results from this study uncovered potential effects of nicotine on XIIMNs found in rostral and caudal regions of the hypoglossal nucleus.