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Voltage-gated sodium channels (VGSCs) play a critical role for electrical signaling in the nervous system by generating action potentials in neurons.The distribution and expression of VGSCs in Parkinsons disease (PD) have not yet been studied, and it is not known whether there are changes in the expression of VGSCs in PD.Four distinct sodium channel α subunits have been reported to be expressed in mammalian central neurons: Nav1.1, Nav1.2, Nav1.3 and Nav1.6.The expression of Nav1.6 is at a high density in the CNS.The distribution and expression of Nav1.6 in the 6-hydroxydopamine lesion rat of PD model were investigated.Immunostaining revealed that Nav 1.6 is exclusively distributed in distinct regions of brain including cerebral cortex, hippocampus, striatum, thalamus, hypothalamus, substantia nigra, cerebellum, etc., in normal rats.Moreover, our results show that Nav1.6 clustered at a high density in the cell membrane and slender processes.In the ipsilateral side of PD model, focal and robust upregulation of Nav 1.6 in the corpus callosum was detected.In addition, the abundance of Nav1.6 in the ipsilateral striatum and substantia nigra was slightly increased, compared to that of the contralateral side.Interestingly, in some brain regions, plaque-like immunoreactivities for Nav1.6 were detected.The alterations of the expression and distribution of Nav 1.6 may provide a novel mechanism involved in the pathogenesis of PD, thus addressing a new therapeutic target and strategy for PD.