| Project/Area Number |
24500461
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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 |
Neurophysiology and muscle physiology
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| Research Institution | Saga University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
FUJITA Tsugumi 佐賀大学, 医学部, 准教授 (70336139)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | オキシトシン / 鎮痛 / 脊髄後角 / 興奮性シナプス伝達 / 抑制性シナプス伝達 / 脱分極 / ラット / パッチクランプ法 / オキシトシン受容体 / ホスホリパーゼC / IP3誘起Ca2+放出 |
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| Outline of Final Research Achievements |
We examined how oxytocin affects synaptic transmission in substantia gelatinosa (SG) neurons by applying the patch-clamp technique to the SG neurons of adult rat spinal cord slices. Bath-applied oxytocin unaffected excitatory transmission while producing an inward current at -70 mV and enhancing spontaneous inhibitory transmission. These activities were mimicked by oxytocin-receptor agonist. The oxytocin current was inhibited by oxytocin-receptor antagonist, U-73122, 2-aminoethoxydiphenyl borate but not dantrolene, chelerythrine, dibutyryl cyclic-AMP and tetrodotoxin, while the spontaneous inhibitory transmission enhancement was depressed by tetrodotoxin. It is concluded that oxytocin produces a membrane depolarization mediated by oxytocin receptors, which increases neuronal activity, resulting in the enhancement of inhibitory transmission, a possible mechanism for antinociception. This depolarization is possibly mediated by phospholipase C and IP3-induced Ca2+-release.
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