2004 Fiscal Year Final Research Report Summary
Role of paracrine mechanism on the excitability of trigeminal root ganglion following temporomandibular joint disorder
| Project/Area Number |
15591980
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | The Nippon Dental University |
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Principal Investigator |
TAKEDA Mamoru The Nippon Dental University, School of Dentistry at Tokyo, Associate Professor, 歯学部, 助教授 (20227036)
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| Project Period (FY) |
2003 – 2004
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| Keywords | trigeminal root ganglion / NK1 receptor / inflammation / paracrine / perforated-patch clamp / Iontophoresis / extracellular recording / Substance P |
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| Research Abstract |
The aim of the present study to investigate whether the local release of substance P (SP) from the trigeminal root ganglion (TRG) neurons innervating temporomandibular joint (TMJ) modulates the excitability of Aβ-TRG neurons innervating the facial skin via the paracrine mechanism, in rats after TMJ inflammation. Complete Freund's adjuvant (CFA) was injected into the rat TMJ to produce inflammation. To compare the difference of SP responsiveness between naive and inflamed rats, we have conducted following experiments by using behavioral (mechanical stimulation threshold), electrophysiological (patch-clamp / extracellular recording with iontophoretic application for TRG neurons), molecular (mRNA for NK1) and immunohistochemical (functional protein for SP/NK1 receptor) approaches. The threshold for escape from mechanical stimulation applied to the orofacial area in TMJ-inflamed rats was significantly decreased. The number of SP-immunoreactive TMJ neurons in the inflamed rats was significa
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ntly increased. In cutaneous medium- and large-diameter TRG neurons (>30μm), the occurrence of SP (100nM) induced membrane depolarization in inflamed rats was larger than that in the naive rats. Quantitative single-cell reverse transcription-polymerase chain reaction analysis showed the increased expression of mRNA for NK1 receptor in cutaneous TRG neurons in inflamed rats. The numbers of SP/NK1 receptors / neurofilament 200 positive cutaneous TRG neurons in the inflamed rats were significantly increased. The mechanical stimulation threshold of Aβ-TRG neurons in inflamed rats was significantly lower than that in naive rats. There were no significant differences on the mechanical stimulation threshold between naive and inflamed rats after iontophoretic application of NK1 receptor antagonists. These results suggest that TMJ inflammation can alter the excitability of Aβ-TRG neurons innervating the facial skin, and that an increase in SP / NK1 receptors in their soma may contribute to the mechanism underlying the trigeminal inflammatory allodynia in the TMJ disorder. Less
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Research Products
(2 results)
