Here, we show that chronic, episodic perinatal nicotine exposure alters nicotinic acetylcholine receptor (nAChR) function, hypoglossal motor neuron (XIIMN) intrinsic properties, and respiratory-related tongue muscle function in vivo. These findings, while similar to what has been shown using a previous model studying chronic, sustained nicotine exposure, are unique in that they are prominent at a critical period in brain development in rodents and reveal important mechanisms that further link perinatal nicotine exposure to altered brain development and the pathophysiology of SIDS. The gene discussed is CHRNA4; the disease is sudden infant death syndrome.