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To understand the molecular basis of neuronal excitation in the mammalian olfactory system, we conducted a systematic analysis of the organization of voltage-gated sodium (Na v ) channel subunits in the main olfactory epithelium (MOE) and vomeronasal organ (VNO) of adult mice. We also analyzed changes in Na v  channel expression during development in these two systems and during regeneration of the MOE. Quantitative PCR shows that Na v 1.7 is the predominant isoform in both adult MOE and VNO. We detected pronounced immunoreactivity for Na v 1.7 and Na v 1.3 in axons of olfactory and vomeronasal sensory neurons (VSNs). Analysis of Na v 1.2 and Na v 1.6 revealed an unexpected subsystem-specific distribution. In the MOE, these Na v  channels are absent from olfactory sensory neurons (OSNs) but present in non-neuronal olfactory cell types. In the VNO, Na v 1.2 and Na v 1.6 are confined to VSNs, with Na v 1.2-immunoreactive somata solely present in the basal layer of the VNO. The subcellular localization of Na v 1.3 and Na v 1.7 in OSNs can change dramatically during periods of heightened plasticity in the MOE. During the first weeks of development and during regeneration of the olfactory epithelium following chemical lesion, expression of Na v 1.3 and Na v 1.7 is transiently enhanced in the somata of mature OSNs. Our results demonstrate a highly complex organization of Na v  channel expression in the mouse olfactory system, with specific commonalities but also differences between the MOE and the VNO. On the basis of their subcellular localization, Na v 1.3 and Na v 1.7 should play major roles in action potential propagation in both MOE and VNO, whereas Na v 1.2 and Na v 1.6 are specific to the function of VSNs. The plasticity of Na v  channel expression in OSNs during early development and recovery from injury could reflect important physiological requirements in a variety of activity-dependent mechanisms.

Organization and Plasticity of Sodium Channel Expression in the Mouse Olfactory and Vomeronasal Epithelia