The sodium channel Nav1.7 is involved in paclitaxel-induced peripheral neuropathy though ERK1/2 signaling in rats.

BACKGROUND Paclitaxel treatment is a major cause of chemotherapy-induced peripheral neuropathy. The sodium channel Nav1.7 plays a critical role in pain perception. However, whether Nav1.7 in the dorsal root ganglion (DRG) is involved in paclitaxelinduced peripheral neuropathy remains unclear. Thus, our study aimed to evaluate whether Nav1.7 participates in the pathogenesis of paclitaxel-induced neuropathy. METHODS Paclitaxel-induced peripheral neuropathy was generated by intraperitoneal administration of paclitaxel on four alternate days. RESULTS The results showed that DRG mRNA and protein expression levels of Nav1.7 were upregulated between days 7 and 21 after administration of paclitaxel. In addition, paclitaxel up-regulated extracellular signal-regulated kinase (ERK1/2) phosphorylation in DRG. Intrathecal injection of U0126 (a MEK inhibitor) blocking ERK1/2 phosphorylation blunted up-regulation of Nav1.7 in the DRG and correspondingly attenuated hyperalgesia. CONCLUSION These results indicated that the sodium channel Nav1.7 in the DRG exerted an important function in paclitaxel-induced neuropathy, which was associated with ERK phosphorylation in neurons.

• Publication year

  2020

• Venue

  Current Neurovascular Research

• Publication date

  2020-05-14

• Fields of study

  Medicine

• Identifiers
  DOI 10.2174/1567202617666200514113441PMID 32407275
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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