| Project/Area Number |
22500296
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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 |
Neuroscience in general
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| Research Institution | Showa University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
IKEDA Keiko 自治医科大学, 医学部, 准教授 (10265241)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 呼吸中枢 / 延髄 / 中枢化学受容器 / Phox2b / 呼吸リズム形成 |
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| Research Abstract |
It has been suggested that Phox2b expressing cells including pFRG/Pre-I neurons in the rostral ventrolateral medulla function as the central chemoreceptors (i.e. CO2 sensor). In the present study, we investigated neuronal mechanisms of high CO2 reception of pFRG/Pre-I neurons, using the brainstem-spinal cord preparation from newborn rats. The CO2 sensitivity of pFRG/Pre-I neurons was preserved even after blockade of Na+channels and Ca2+channels, and the membrane depolarization induced by hypercapnic stimulation was mainly due to the closing of K+channels. We also found that Phox2b-expressing cells including pFRG/Pre-I neurons in the parafacial region of the rostral ventral medulla tended to assemble around capillary blood vessels. We confirmed that TASK1,2 and 3 channels were less significantly involved in hypercapnic responses of pFRG/Pre-I neurons. Our findings demonstrate that the pFRG/Pre-I neurons possess postsynaptic mechanisms that are directly responsible to high CO2 stimulation.
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