1995 Fiscal Year Final Research Report Summary
Studies on neurotransmitters and neural mechanisms involved in respiratory rhythmogenesis
| Project/Area Number |
05680672
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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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 |
TAKEDA Ryuji Toyama M-P U., Pharmacology, Professor, 医学部, 教授 (80020791)
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| Co-Investigator(Kenkyū-buntansha) |
OKAZAKI Mari Toyama M-P U., Pharmacology, Res. Associate, 医学部, 助手 (50272901)
HAJI Akira Toyama M-P U., Pharmacology, Assoc. Professor, 医学部, 助教授 (50228433)
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| Project Period (FY) |
1993 – 1995
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| Keywords | Respiratory center / Rhythmogenesis / Respiratory neuron / Postsynaptic potentials / NMDA receptors / AMPA receptors / GABA-A receptors / Vagus nerve |
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| Research Abstract |
Systemic application of dizocilpine, a non-competitive blocker of NMDA receptors, produced an apneustic breathing in vagotomized cats. This breathing pattern was characterized by a prolonged inspiratory phase, reflecting an extreme delay of the inspiratory off-switch (10S) process. Intracellular recordings together with measurements of input resistance from bulbar respiratory neurons revealed that the blockade of NMDA receptors in the respiratory network disfacilitated inspiratory (I) and post-inspiratory (PI) neurons during their active (depolarizing) phase and disinhibited during their inactive (hyperpolarizing) phase. Stimulation of vagus nerves induced I0S both in eupnea and in dizocilpine-induced apneusis. This peripherally-stimulated I0S was associated with a series of postsynaptic potentials (PSPs) evoked in bulbar respiratory neurons. In I neurons the evoked EPSPs increased in amplitude and the evoked IPSPs decreased, while both types of PSPs evoked in PI neurons unchanged during dizocilpine-induced apneusis. The peripherally-evoked EPSPs were shown to be mediated through AMPA receptors and the evoked IPSPs through GABA-A receptors.
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