| Project/Area Number |
07044238
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Institution | Toyama Medical and Pharmaceutical University |
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Principal Investigator |
TAKEDA Ryuji Toyama Medical and Pharmaceutical University professor, 医学部, 教授 (80020791)
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| Co-Investigator(Kenkyū-buntansha) |
JACQUIN Thierry C.N.R.S./Institute Alfred Fessard/Gif-sur-Yvette Director, Director
CAHMPAGNAT J CNRS/I.A.F./Neurophysiol., Director
DENAVIT SAUB CNRS/Inst.Alfred Fessard, Chief Dire
OKAZAKI Mari Toyama Medical and Pharmaceutical University Research Assistant, 医学部, 助手 (50272901)
HAJI Akira Toyama Medical and Pharmaceutical University Associate professor, 医学部, 助教授 (50228433)
DENAVIT SAUBIE Monigue C.N.R.S./Institute Alfred Fessard/Gif-sur-Yvette Chief Director
CHAMPAGNAT Jean C.N.R.S./Institute Alfred Fessard/Gif-sur-Yvette Director
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| Project Period (FY) |
1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1995: ¥3,100,000 (Direct Cost: ¥3,100,000)
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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 administration of dizocilpine, a non-competitive antagonist 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 (IOS) 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 postinspiratory (PI) neurons during their active (depolarizing) phase and disinhibited during their inactive (hyperpolarizing) phase. Stimulation of vagus or superior laryngeal nerves induced IOS both in eupnea and in dizocilpine-induced apneusis. This peripherally-induced IOS 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. Additionally, the peripherally-evoked EPSPS were shown to be mediated through AMPA receptors and the evoked IPSPs through GABA-A receptors.
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