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Assessment of Nerve Injury-Induced Mechanical Hypersensitivity in Rats Using an Orofacial Operant Pain Assay
Published on: July 26, 2022
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N/OFQ modulates orofacial pain induced by tooth movement through CGRP-dependent pathways
Xinyu Yan1, Han Han1, Shizhen Zhang1
1Department of Orthodontics, State Key Laboratory of Oral Diseases, National Clinical Center for Oral Research, West China Hospital of Stomatology, Sichuan University, No. 14, Section 3, Ren Min Nan Road, Chengdu, 610041, China.
BMC Neuroscience
|April 10, 2021
Summary
Nociceptin/orphanin FQ (N/OFQ) exacerbates orofacial pain by increasing calcitonin gene-related peptide (CGRP) levels. N/OFQ-based gene therapy also amplified pain and CGRP expression in trigeminal ganglia.
Area of Science:
- Neuroscience
- Pain Research
- Molecular Biology
Background:
- Nociceptin/orphanin FQ (N/OFQ) exhibits dual roles in modulating orofacial pain.
- Calcitonin gene-related peptide (CGRP) is recognized for its pro-nociceptive effects in orofacial pain.
Purpose of the Study:
- To investigate the impact of N/OFQ on orofacial pain modulation.
- To determine the effect of N/OFQ on CGRP release in the context of orofacial pain.
Main Methods:
- An orofacial pain model was created in rats by simulating tooth movement.
- N/OFQ expression and pain levels were assessed; N/OFQ receptor agonist/antagonist effects on pain and CGRP in trigeminal ganglia (TG) were evaluated.
- Gene therapy was employed to overexpress N/OFQ, validating its modulatory role.
Main Results:
- Tooth movement induced orofacial pain and elevated N/OFQ expression.
- N/OFQ worsened pain and increased CGRP expression in TG; UFP-101 (antagonist) reduced pain and CGRP levels.
- N/OFQ gene therapy successfully increased N/OFQ in TG, leading to exacerbated pain and elevated CGRP.
Conclusions:
- N/OFQ appears to intensify orofacial pain.
- This exacerbation is potentially mediated by the upregulation of CGRP.
- Findings highlight N/OFQ's role in orofacial pain pathways involving CGRP.
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