Postnatal nicotine effects on the expression of nicotinic acetylcholine receptors in the developing piglet hippocampus and brainstem.

摘要: Postnatal exposure to cigarette smoke during infancy is associated with increased number of respiratory illnesses, impaired pulmonary function, and the occurrence Sudden Infant Death Syndrome (SIDS). It also reduced cognitive functioning attention deficits in childhood. Nicotine, major neurotoxic component smoke, induces its actions by binding nicotinic acetylcholine receptors (nAChR). Using a piglet model postnatal nicotine exposure, we studied immunohistochemical expression nAChR subunits α2, α3, α4, α5, α7, α9, β1 β2 brainstem medulla hippocampus, given role these structures cardiorespiratory control cognition, respectively. We compared piglets exposed postnatally 2mg/kg/day for 14 days (n=14: 7 males: females) controls females). In decreased was seen α3 CA1 (p=0.017), α9 (p<0.001) CA2 (p<0.001), (p=0.001) CA3 (p=0.036). medulla, nucleus spinal trigeminal tract had α2 α4; vestibular hypoglossal β1; dorsal motor vagus α4 β1. This first demonstration that non-classical are affected developing brain, implications discussed.