Elucidation of intracellular signal of opioid-induced itching and TRPA1-itch signal interaction

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K20084
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Anesthesiology
• Research Institution: Niigata University
• Principal Investigator: SASAKI MIKA 新潟大学, 医歯学総合病院, 技術補佐員 (20774061)
• Research Collaborator: KAMIYA Yoshinori 新潟大学, 医歯学系, 准教授
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: オピオイド誘発性痒み / セロトニン受容体 / オンダンセトロン / ガストリン放出ペプチド / MAPキナーゼ

Outline of Final Research Achievements

The intrathecal administration of 30 nmol morphine increased the itching behavior of mice, and elevated the phosphorylation level of ERK and p38 of MAP kinase, which known to be associated with pain and itch at the dorsal horn of the spinal cord. At the same time, immunohistochemistry confirmed an increase in gastrin releasing peptides, which are histamine-independent itching substances, in the dorsal horn I and Ⅱ layer of the spinal cord and DRG. On the other hand, the itching behavior of mice by intrathecal administration of morphine was significantly suppressed by pre-administration of a 5-HT3 receptor antagonist ondansetron and pre-administration of serotonin synthase inhibitor p-chrolophenylalanine. These results suggested that activation of serotonin receptor, particularly 5-HT3 receptor, was involved in itching by morphine.

Free Research Field

痛み