| Project/Area Number |
15590827
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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 |
Respiratory organ internal medicine
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| Research Institution | Keio University |
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Principal Investigator |
OYAMADA Yoshitaka Keio University, Department of Medicine, Assistant, 医学部, 助手 (00233627)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIZAKA Akitoshi Keio University, Department of Medicine, Professor, 医学部, 教授 (90176181)
山口 佳寿博 慶應義塾大学, 医学部, 助教授 (30129712)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2004: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Central ventilatory chemosensitivity / Inwardly rectifying potassium channel / IRK subfamily / 呼吸 |
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| Research Abstract |
Chemosensitive neurons - neurons which change their electrical activity in response to a shift of PCO_2/pH, independent of chemical synaptic transmission - are widely distributed in the brainstem. These neurons could be CO_2/pH-sensors far central ventilatory chemosensitivity. Among inwardly rectifying potassium channel(Kir) subfamilies, Kir2x(IRK) subfamily is expressed mainly in neurons and cardiomyocytes, and is believed to be involved in setting their membrane potentials. Some Kirs are reported to change their conductance responding to intracellular acidification(Xu et al., 2000; Zhu et al., 2000). Therefore, electrical responses of chemosensitive neurons to PCO_2/pH could be determined by some IRK(s). The purpose of this project is to invesligate the roles of IRK(s) in central ventilatory chemosensitivity. The project consists of 1)identification of IRK expressed in locus ceruleus neurons and respiratory neurons in the isolated brainstem-spinal cord preparation of the neonatal rat, which have already been proved to be chemosensitive, 2)determination of chemosensitivity of identified IRK. Although final results have not been obtained yet, we have recently demonstrated that Kir2.2 is transiently involved in hypercapnic ventilatory response of the mouse during postnatal development (Oyamada et al., 2005).
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