| Project/Area Number |
12680749
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Toyama Medical and Pharmaceutical University |
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Principal Investigator |
HAJI Akira Toyama Medical and Pharmaceutical University, 医学部, 助教授 (50228433)
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| Co-Investigator(Kenkyū-buntansha) |
岡崎 真理 富山医科薬科大学, 医学部, 助手 (50272901)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | neuronal network / respiratory neuron / NMDA mechanism / pneumotaxic center / synaptic inputs / vagal afferents / ryanodine受容体 / 細胞内記録 / NPBM / 迷走神経 |
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| Research Abstract |
To investigate integration and modulation of synaptic inputs in the central rhythm generation network, membrane potential, action potential and postsynaptic potentials were recorded from bulbar respiratory neurons in decerebrate, unanesthetized, vagotomized, artificially ventilated cats. The following results were obtained.
1. Synaptic inputs from the pulmonary afferents and the pontine pneumotaxic center (nucleus parabrachialis medialis : NPBM) were conveyed on the central respiratory neurons through different pathways but transmitted in a similar manner. These inputs were modulated by NMDA receptor mechanisms. Especially, the NMDA mechanisms are assumed to augment and/or synchronize the late-inspiratory depolarization and discharge of late-I neurons, leading to GABA release and consequently off-switching of bulbar inspiratory neurons and phrenic motoneurons. Therefore, the NMDA-mediated sequential depolarization of late-I and post-I neurons plays an essential role in IOS. During apneusis evoked by blockade of NMDA receptors, IOS was induced by non-NMDA-mediated rapid excitation of late-I and post-I neurons, which was followed by excitation of aug-E neurons.
2. Respiratory neurons were identified by intracellular recording of membrane potential and by intracellular labeling with neurobiotin. These neurons were examined distribution of glutamic acid decarboxylase or NMDA receptors by double immunofluorescent staining. All types of propriobulbar respiratory neurons are GABAergic. NMDA receptors are distributed in lesser degree in bulbospinal aug-E neurons than in other types of neurons.
3. Ca^<2+> derived from ryanodine-sensitive Ca^<2+> stores modulates the synaptically induced periodic membrane potential fluctuations and burst activity in respiratory neurons through activating the Ca^<2+>-dependent K^+ channels.
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