The Effect of Prenatal Nicotine Exposure on Ventilation Parameters and Receptor Expression in the Neonatal Rat Brainstem

Abstract

Prenatal nicotine exposure has recently been linked to respiratory dysfunction in infants and has been named one of the largest contributing factors in Sudden Infant Death Syndrome. Experiments were performed using the neonatal rat model to determine the mechanism behind the link between prenatal nicotine exposure and respiratory dysfunction, clinically manifesting itself as SIDS. Protocol called for full body plethysmography to be performed on nicotine exposed or saline exposed neonates on postnatal days 1, 3, 6, 9, 12, 18 and 21. However, a dysfunctioning apparatus impeded ventilation procedures. Animals were then transcardially perfused, postfixed and brains were dissected. Medullas were cut into 40 μm transverse slices and mounted on electrostatic slides. Immunohistochemistry was used to fluorescently tag cells containing important structure and receptors within the medulla including NeuN, NK-1R, nAChR, GABA-AR and Glutamate AMPAR. Cells were visualized for receptor expression and receptor density in control animals vs. PNE animals was studied. Needed changes in protocol prevented conclusive findings that established the relationship in question. These changes included the use of Trizma buffer over PBS and the reduction in the concentration of the fluorescent secondary antibodies used. However these changes will prove to be useful information in further experiments.