TRPV2 is required for mechanical nociception and the stretch-evoked response of primary sensory neurons

Kimiaki Katanosaka, Satomi Takatsu, Kazue Mizumura, Keiji Naruse, Yuki Katanosaka

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Mechanotransduction plays important roles in many sensory processes, including touch, pain, hearing, and proprioception. However, the molecular mechanisms of mechanical nociception have remained unclear. Here, we showed that elimination of transient receptor potential vanilloid 2 (TRPV2) in mice resulted in the deficit of mechanical nociception due to the lack of mechanosensitivity in a subclass of adult primary sensory neurons (PSNs). The PSN-specific TRPV2-deficient mice showed behavioural impairment of mechanical nociception in tail-pressure and von Frey hair tests, without defects in axonal growth and neuronal composition. Conversely, the mice displayed normal behaviour to noxious heat and non-noxious tactile stimuli. Furthermore, based on the stretch-evoked Ca2+ response of cultured PSNs, we characterised two types of stretch-activated neurons in normal mice; fast-decay high-threshold and slow-decay low-threshold mechanosensitive. The cultured neurons from TRPV2-deficient mice lacked stretch-evoked Ca2+ responses by fast-decay neurons normally activated by high-threshold mechanical stimulation. These results demonstrated that TRPV2 has a critical role in mechanical nociception in the adult somatosensory system.

Original languageEnglish
Article number16782
JournalScientific Reports
Volume8
Issue number1
DOIs
Publication statusPublished - Dec 1 2018

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TRPV Cation Channels
Nociception
Sensory Receptor Cells
Touch
Neurons
Proprioception
Hair
Hearing
Tail
Hot Temperature
Pressure
Pain
Growth

ASJC Scopus subject areas

  • General

Cite this

TRPV2 is required for mechanical nociception and the stretch-evoked response of primary sensory neurons. / Katanosaka, Kimiaki; Takatsu, Satomi; Mizumura, Kazue; Naruse, Keiji; Katanosaka, Yuki.

In: Scientific Reports, Vol. 8, No. 1, 16782, 01.12.2018.

Research output: Contribution to journalArticle

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