| Project/Area Number |
26861561
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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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 |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 三叉神経節 / 炎症性疼痛 / GABA / GAD / 痛覚過敏 / 関連痛 / 非歯原性歯痛 / ＧＡＢＡ / ＧＡＤ / 侵害受容 / GABA A / GABA B |
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| Outline of Final Research Achievements |
This study was aimed at elucidating changes in the expression of GABA-ergic neurons of TRG in rats which showed hyperalgesia and/or allodynia by artificially-induced chronic inflammation in their TMJ and facial skin. Although GABA is a main inhibitory neurotransmitter in the CNS, little is known about the role in the PNS, including TRG. We compared GAD67 expression of TRG neurons in rats with and without TMJ and facial skin inflammations. In the FG labeled TRG neurons, the proportion of GAD67 immunoreactive cells of EXP group was 16.0%, which was about twice as much as that seen in CONT group. In addition, by using extracellular recording, it was found that microiontophoretically applied baclofen inhibited TRG neurons excitation in pentobarbital-anesthetized rat.
Taken together, our results suggest that hyperalgesia and/or allodynia due to orofacial chronic inflammation may be related at least in part to the up-regulation of GAD67-positive GABA-ergic neurons in the TRG.
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