Developmental nicotine exposure (DNE) is known to cause abnormal development of multiple brain regions and results in impaired control of breathing and altered behaviors that rely on proper coordination of the muscles of the tongue. The adverse effects of nicotine are presumably caused by its actions on nicotinic acetylcholine receptors (nAChRs), which modulate fast-synaptic transmission and play a prominent role during brain development. Previous work has shown that DNE alters nAChR function in multiple brainstem regions (Pilarski et al., 2012, Wollman et al, 2016). Moreover, DNE causes multiple changes to XIIMNs, which innervate the muscles of the tongue (Powell et al., 2016, Powell et al., 2015, Pilarski et al., 2011). These changes likely reflect both altered development as a primary outcome of the chronic presence of nicotine, as well as, homeostatic adjustments made in an attempt to maintain normal motoneuron output. With the experiments described here, we tested the hypothesis that DNE alters the development of fast-synaptic transmission to XIIMNs, which, along with intrinsic properties of these neurons, is a main determinant of motor output to the muscles of the tongue. Additionally, we tested the hypothesis that DNE alters the function of nAChRs located on multiple brainstem neurons, including those that modulate fast-synaptic transmission to XIIMNs. For these experiments, we used whole cell patch clamp recordings from XIIMNs in a transverse slice of the medulla, and extracellular recordings from the 4th cervical ventral root in the brainstem spinal cord, split bath preparation. All preparations were obtained from control or DNE neonatal rats in the first week of life. Overall, the results of these experiments show that DNE alters fast-synaptic transmission to XIIMNs, which likely reflects appropriate homeostatic adjustments aimed at maintaining normal motor output at rest. However, these results also show that nAChR function is significantly altered by DNE, indicating fast-synaptic transmission may not be appropriately modulated in response to increased release of acetylcholine (ACh), the endogenous neurotransmitter for nAChRs.