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논문 기본 정보

자료유형
학술저널
저자정보
Seon-Hui Jang (Postdoc Research Assistant Department of Oral Physiology School of Dentistry & Institute of Oral Bioscience Jeonbuk National University Jeonju Republic of Korea) Dong-Hyu Cho (Department of Obstetrics and Gynecology Jeonbuk National University Medical School Research Institute of Clinical Medicine of Jeonbuk National University-Biomedical Research Institute of Jeonbuk Natio) Seong-Kyu Han (Department of Oral Physiology School of Dentistry & Institute of Oral Bioscience Jeonbuk National University Jeonju Republic of Korea)
저널정보
조선대학교 치의학연구원 Oral Biology Research Oral Biology Research 제47권 제2호
발행연도
2023.6
수록면
43 - 50 (8page)
DOI
10.21851/obr.47.02.202306.43

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초록· 키워드

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The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) receives orofacial nociceptive information from primary afferent neurons and transmits this information to higher brain centers. Resveratrol (3, 5, 4′-trihydroxystilbene) is a polyphenolic compound found in various plant species and have been reported to have various biological activities, including analgesic effects. Although many studies have investigated the mechanism of action of resveratrol in terms of its antinociceptive effect, limited research has been conducted on the effects of resveratrol on SG neurons involved in orofacial pain transmission, especially to understand its relevance to glutamate receptors. To address this research gap, the present study investigated the effect of resveratrol on glutamate receptor activity in SG neurons using the whole-cell patch-clamp technique. The results showed that resveratrol significantly inhibited glutamate-mediated inward currents in SG neurons. Notably, there were no changes in α-amino-3-hydroxy-5-methyl-4- isoxazolepropionic acid- or kainic acid-mediated inward currents in the presence of resveratrol, although N-methyl-D-aspartate (NMDA)-mediated inward currents were markedly suppressed. Taken together, these results suggest that resveratrol may be involved in orofacial pain transmission in SG neurons of the Vc by inhibiting the activity of NMDA receptors, among ionotropic glutamate receptors.

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