The basal thermal sensitivity of the TRPV1 ion channel is determined by PKCβII

Lin Li, Raquibul Hasan, Xuming Zhang

Research output: Contribution to journalArticlepeer-review


Peripheral nociceptors are excited by the activation of membrane receptors and ion channels. The heat-sensitive TRPV1 ion channel responds to various noxious chemical and thermal stimuli, causing pain and itch. Here, we show that TRPV1 is coexpressed with PKCβII in a subset of mouse sensory neurons and that, in these neurons, TRPV1 binds directly to PKCβII, leading to the activation and translocation of PKCβII. Activated PKCβII, in turn, significantly increases the responsiveness of TRPV1 by phosphorylating Thr705. The heat sensitivity of TRPV1 is almost eliminated by either knocking down PKCβII or mutating Thr705; however, neither of these manipulations affects the potentiation of TRPV1 caused by the activation of PKCε. PKCβII thus acts as an auxiliary subunit of TRPV1 by forming a population-dependent TRPV1 ion channel complex controlling the sensitivity of TRPV1 and setting the threshold for pain and itch.

Original languageEnglish
Pages (from-to)8246-8258
Number of pages13
JournalJournal of Neuroscience
Issue number24
Publication statusPublished - 11 Jun 2014


  • Capsaicin
  • cultured cells
  • Down-regulation
  • spinal ganglia
  • green fluorescent proteins
  • hot temperature
  • membrane potentials
  • mutation
  • phosphorylation
  • protein binding
  • protein Kinase C beta
  • Rats,
  • sensory system agents
  • TRPV cation channels


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