Role of Axonal Translation in the Upregulation of Nav1.1 Following Nerve Injury

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      Recent data indicates that an increase in axonal NaV1.1 enables action potential (AP) propagation in a subpopulation of axons in the trigeminal nerve following injury, and that selective block of this channel can attenuate chronic constriction injury (CCI)-induced mechanical hypersensitivity. The increase in axonal NaV1.1 is not associated with an increase in protein or mRNA in the trigeminal ganglion (TG), suggesting this upregulation is due to stabilization, local translation, or increased trafficking. The goal of present study to begin to assess contribution of local translation as well as identify the afferent subpopulation(s) in which the increase occurs. To address this, quantitative RT-PCR and Western blot (WB) of the infra-orbital nerve (ION) with and without pharmacological manipulations translation and trafficking were initiated. To enable analysis of afferent subpopulations in which NaV1.1 was upregulated, GCaMP6s expression in trigeminal ganglia was induced by AAV injection in neonatal rats. Results from this series of experiments confirms that mRNA is detectable in the ION, consistent with previous data reported by Korczeniewska et al (Eur. J Pain 2020, PMID: 32100907), though no apparent differences were observed with CCI-ION. Additionally, neonatal AAV9-GCaMP6s injection provided robust expression throughout the TG for in-vivo imaging. The absence of a detectable decrease in axonal NaV1.1 mRNA is consistent with an increase in mRNA trafficking to compensate for an increase in local translation. Ongoing experiments will be used to confirm these initial observations. Grant support from 1F31NS125993-01.
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