| Project/Area Number |
17591944
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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 | Kyushu Dental College |
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Principal Investigator |
HONDA Eiko Kyushu Dental College, Physiology, Special trainees, 歯学部, 特別研修員 (00047812)
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| Co-Investigator(Kenkyū-buntansha) |
INENAGA Kiyotoshi Kyushu Dental College, Physiology, Professor, 歯学部, 教授 (90131903)
ONO Kentaro Kyushu Dental College, Physiology, Assistant Professor, 歯学部, 助手 (40316154)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2005: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | oral dryness / central noradrenaline / subfornical organ / patch clamp / a receptor / rat / slice nrenaration / ノルアドレナリン / パッチクランプ / フェニレフリン / アドレナリン受容体 / 抑制性シナプス後電流 / コンダクタンス |
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| Research Abstract |
Activation of the subfornical organ (SFO) induces drinking behavior, that is, oral dryness. In this study, the effects of NA and its analogues on SFO neurons in rat slice preparations were investigated by using whole cell patch clamp recording. In the current clamp mode, the application of NA at 10-100 μM produced membrane depolarization (63%, 17 responsive neurons /27 neurons tested) and hyperpolarization (22%, 6/27 neurons). In the voltage clamp mode, NA application at 1-100 μM produced inward currents (69%, 42/61 neurons) and outward currents (23%, 14/61 neurons). These currents were remained in the presence of TTX or in the coapplication of glutamate and GABA receptor antagonists. In most of the neurons (25/31 neurons) showing inward currents in the presence of NA, the membrane conductance was not changed by voltage ramps or hyperpolarizing pulse stimulation. Similar responses were obtained by the application of the αl agonist phenylephrine. The phenylephrine-induced inward currents were inhibited by the α1 antagonist prazosin. In addition, the α2 agonist clonidine decreased the frequency of spontaneous GABAergic inhibitory postsynaptic currents (4/10 neurons). The results suggest that SFO neurons in rats are activated postsynaptically through α1 adrenoceptors, and that the activation is enhanced by suppressing GABAergic inhibitory synaptic inputs through presynaptic α2 adrenoceptors.
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