1998 Fiscal Year Final Research Report Summary
Phase switching of respiratory rhythm in bulbar respiratory neuronal network
| Project/Area Number |
09680761
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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 TMPU,Pharmacology, Associate Professor, 医学部, 助教授 (50228433)
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| Co-Investigator(Kenkyū-buntansha) |
OKAZAKI Mari TMPU,Pharmacology, Research Associate, 医学部, 助手 (50272901)
TAKEDA Ryuji TMPU,Pharmacology, Professor, 医学部, 教授 (80020791)
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| Project Period (FY) |
1997 – 1998
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| Keywords | respiratory rhythm generation / respiratory neuron / NMDA receptor / GABA receptor / inspiratory off-switch / inspiratory on-switch |
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| Research Abstract |
To investigate the phase transitional process of respiratory rhythm generation, inspiratory off-switching (LOS) and on-switching (IonS), membrane potential and postsynaptic potentials were recorded from bulbar respiratory neurons in decerebrate, unanesthetized, vagotomized, artificially ventilated cats. The following results were obtained.
1. Eupneic respiration was generated within the bulbar respiratory neuronal network without pulmonary afferent inputs and pontine pneumotaxic inputs.
2. During IOS, a sequential excitation of late-I neurons and P1 neurons inhibited the inspiratory activity of aug-I neurons. Blockade of NMDA receptors resulted in apneusis by impairing this lOS mechanism. During apneusis, IOS was induced by excitation of E2 neurons through activation of non-NMDA receptors.
3. During IOS, the final inhibitory transmission to aug-I neurons was mediated by the GABA-A receptor mechanism.
4. Short latency postsynaptic potentials were evoked in bulbar respiratory neurons during IOS induced by vagal stimulation. These postsynaptic responses were similar to those during the vagally induced IonS.
5. Low-threshold Ca currents involved in the rebound depolarization of respiratory neurons at the transitional phase from the inactive phase to the active phase.
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