2000 Fiscal Year Final Research Report Summary
Neuronal mechanisms of development of respiratory neuron network in the late fetal stage of rat
| Project/Area Number |
10680753
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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 |
ONIMARU Hiroshi Showa Univ.School of Medicine, Associate., Professor, 医学部, 助教授 (30177258)
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| Project Period (FY) |
1998 – 2000
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| Keywords | respiratory center / development / fetal stage / rat / brainstem-spinal / respiratory neuron / amine / GABA |
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| Research Abstract |
We analyzed development of respiratory center in the late fetal stage (E16-21), using rat fetus brainstem-spinal cord preparations. [1] In addition to increase in frequency and amplitude of respiratory nerve discharge from fourth cervical ventral roots, the burst pattern changed markedly during the late fetal development. Namely, duration of inspiratory phase after E19-20 increased 2-3 times or more (>400 ms) compared with short burst duration (100-200 ms) before E19. Subtypes of respiratory neurons (pre-inspiratory, three types of inspiratory, expiratory ; neonatal type network) similar to those in newborn rats were found in the ventrolateral medulla of preparations from E21/20 and in some E19 rats. Before E18, the presence of such subtypes of respiratory neurons was not clear (fetal type network). Many respiratory neurons in fetal type network possess properties as intrinsic burster, and they were classified into inspiratory neurons and neurons receiving inhibition during inspiratory
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phase. [2] Amines (adrenaline, 5-HT, dopamine) or cAMP-related substances (forskolin, PACAP) prolonged the burst duration of C4 inspiratory activity and converted reversibly the network property from neonatal type to fetal type. Prototype of type-I inspiratory neurons which were burster or non-burster was found even in E17. Intrinsic burster neurons inhibited during inspiratory phase were proposed as a candidate of prototype of pre-inspiratory neurons. [3] Cl^--dependent synaptic potentials in medullary respiratory neurons caused a membrane hyperpolarization even at E16. Bath-applied GABA (0.2-1 mM) mainly induced a depolarization of fetal respiratory neurons in high or low Cl^-/gramicidin recordings. In low Cl^-/whole-cell recordings, GABA induced a membrane depolarization in 74% neurons. Most responses to GABA were accompanied by a marked reduction in the membrane resistance and a loss of membrane excitability. Effects of GABA (0.5 -1 mM) were blocked by 100 μM bicuculline. GABA-induced depolarization reduced by 30-40% in CO_2/HCO_3^- free-HEPES buffered solution. Less
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[Publications] Shirasawa, S., Arata, A., Onimaru, H., Roth, K.A., Brown, G.A., Horning, S., Arata, S., Okumura, K., Sasazuki, T.and Korsmeyer, S.J.: "Rnx (Hox11L2)-deficiency results in congenital central hypoventilation."Nature Genetics. 24. 287-290 (2000)
Description
「研究成果報告書概要(欧文)」より
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