Analysis of pain relief systems at peripheral sensory nerves

KAKEN

About This Project

Japan Grant Number
JP17H03933 (JGN)
Funding Program
Grants-in-Aid for Scientific Research
Funding Organization
Japan Society for the Promotion of Science

Kakenhi Information

Project/Area Number
17H03933
Research Category
Grant-in-Aid for Scientific Research (B)
Allocation Type
  • Single-year Grants
Review Section / Research Field
  • Biological Sciences > Agriculture > Animal life science > Integrative animal science
Research Institution
  • Tottori University
Project Period (FY)
2017-04-01 〜 2021-03-31
Project Status
Completed
Budget Amount*help
16,510,000 Yen (Direct Cost: 12,700,000 Yen Indirect Cost: 3,810,000 Yen)

Research Abstract

We examined whether functional associations between adrenergic systems in peripheral sensory systems and TRPV1 caused analgesia. Although, nociceptive behaviors induced by capsaicin injected into rat hind paws were reduced by noradrenaline (NA) and clonidine, a selective α2 agonist, injected into the same site, they were not affected when adrenergic agents were injected into contralateral hind paws. Immunohistochemical experiments revealed α2 receptors and TRPV1 were co-expressed in the cell body of the primary sensory neurons. Electrophysiological capsaicin responses observed in isolated primary sensory neurons recorded by the patch clamp method were extensively inhibited by NA and clonidine, and these effects were inhibited by yohimbine, a selective α2 antagonist. These results suggest that inhibition of TRPV1 activity by α2 adrenoceptors on sensory peripheral nerve terminals causes the analgesic effect.

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