| Project/Area Number |
25462908
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | National Defense Medical College |
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Principal Investigator |
TASHIRO AKIMASA 防衛医科大学校(医学教育部医学科進学課程及び専門課程、動物実験施設、共同利用研究, 医学教育部医学科専門課程, 助教 (60598118)
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| Research Collaborator |
Bereiter David A ミネソタ大学, 教授
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 痛覚 / エストロゲン / GABA / mGluR / 顎関節 / オピオイド / 顎関節痛 / 代謝型グルタミン酸受容体 / 三叉神経 |
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| Outline of Final Research Achievements |
Arthritis and musculoskeletal disorders, including temporomandibular joint disorder (TMD), are chronic pain conditions that occur more frequently in women of reproductive age than men. However, considerable evidence suggests that estrogen (E2) status plays a significant role. Although E2 acts GABAergic neurons to affect a wide range of functional pathways in the CNS, it is not known if E2 interact GABAergic activity in the brain regions that process nociceptive input from the TMJ. Recent studies indicated that E2-induced IPSC suppression depends on ERa- and mGluR1-dependent mobilization to decrease the probability of GABA release from inhibitory synaptic inputs. In present study we demonstrated that 1) E2 suppressed GABA(A) mediated inhibition 2)E2 acts mGluR1 dependent mechanism to enhance TMJ nociceptive processing by laminae I-II neurons in the medullary dorsal horn.
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