Study of verification and origin of a novel medullary respiratory neuron group (para-facial respiratory group)

一种新型髓质呼吸神经元群(面旁呼吸群)的验证及起源研究

基本信息

  • 批准号:
    16500208
  • 负责人:
  • 金额:
    $ 2.18万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2004
  • 资助国家:
    日本
  • 起止时间:
    2004 至 2006
  • 项目状态:
    已结题

项目摘要

Aim of this study was to reveal cellular level entity (e.g. distribution, morphology, physiological and pharmacological characteristics) and the function of novel medullary respiratory neuron group (para-facial respiratory group, pFRG ; Onimaru & Homma, 2003). For this analysis, we used the brainstem-spinal cord preparation isolated form newborn rats. The present study revealed the following : 1)The pFRG consisted predominantly of pre-inspiratory (Pre-I) neurons. 2)Cell soma of the pFRG/Pre-I neuron was located close to the ventral surface, immediately below the pia membrane, at the level of the facial nucleus. 3)Activity of the pFRG/Pre-I neurons was not inhibited by μ-opiate agonist, DAMGO. 4)Activity of the pFRG/Pre-I neurons was reflected in the facial nerve activity. 5)When the medulla was transversely cut between the pFRG and the pre-Botzinger complex (PBC), each block of the medulla could produced spontaneous rhythmic activity under the appropriate experimental conditions. 6)These rhythmic activity corresponded to the pFRG/Pre-I (in the rostral block) and PBC/inspiratory (in the caudal block) neuron activity. 7)Rhythm of the pFRG/Pre-I neurons was depressed by increasing extracellular potassium ion concentration, application of a persistent sodium channel blocker (riluzole) or lowering CO2 pressure, whereas the PBC/inspiratory activity was more resistant to these manipulations. 8)When the medulla was cut through the midline, rhythmic activity of the pFRG/Pre-I neurons was maintained independently in the right and left medulla, but PBC-inspiratory activity was stopped. These findings showed that mechanism of rhythm generation by the pFRG/Pre-I neurons are essentially different from that of PBC-inspiratory neurons and suggested that the pFRG/Pre-I neurons determine basic respiratory rhythm under normal experimental condition with normal (or lower) external potassium concentration.
本研究的目的是揭示新的延髓呼吸神经元群(面旁呼吸群,pFRG;Onimaru&Homma,2003)的细胞水平实体(如分布、形态、生理和药理学特征)和功能。在这项分析中,我们使用了从新生大鼠身上分离出来的脑干-脊髓标本。本研究发现:1)pFRG主要由吸气前(Pre-I)神经元组成。2)pFRG/Pre-I神经元胞体靠近面神经核腹侧面,紧靠软脑膜下方。3)μ阿片激动剂DAMGO不抑制pFRG/Pre-I神经元的活动。4)面神经活动反映了pFRG/Pre-I神经元的活动。5)当切断延髓位于pFRG和Pre-Botzinger Complex(PBC)之间时,在适当的实验条件下,延髓的每一块都能产生自发的节律性活动。6)这些节律性活动与pFRG/Pre-I(吻侧阻滞)和PBC/吸气(尾侧阻滞)神经元活动相对应。7)增加细胞外钾离子浓度、应用持续性钠通道阻滞剂(利鲁唑)或降低二氧化碳分压可抑制pFRG/Pre-I神经元的节律,而PBC/吸气活动对这些操作更具抵抗力。8)切断延髓中线后,左右两侧延髓内pFRG/Pre-I神经元的节律性活动独立维持,但PBC吸气活动停止。这些结果表明,pFRG/Pre-I神经元的节律产生机制与PBC-吸气神经元的节律产生机制有本质的不同,提示pFRG/Pre-I神经元在正常实验条件下,在正常(或低)外钾浓度的情况下,决定基本的呼吸节律。

项目成果

期刊论文数量(76)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Facilitation of respiratory rhythm by aμ-opioid agonist in newborn rat pons-medulla-spinal cord preparations.
aμ-阿片受体激动剂在新生大鼠脑桥-髓质-脊髓制剂中促进呼吸节律。
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Tanabe A;Fujii T;Onimaru H
  • 通讯作者:
    Onimaru H
Electrophysiological properties of rostral ventrolateral medulla neurons in angiotensin II 1a receptor knockout mice
  • DOI:
    10.1161/01.hyp.0000173421.97463.ac
  • 发表时间:
    2005-08-01
  • 期刊:
  • 影响因子:
    8.3
  • 作者:
    Matsuura, T;Kumagai, H;Saruta, T
  • 通讯作者:
    Saruta, T
In vitro visualization of respiratary neuron activity in the newborn mouse ventral medulla
新生小鼠腹延髓呼吸神经元活动的体外可视化
  • DOI:
  • 发表时间:
    2004
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Onimaru H.;Arata A.;他
  • 通讯作者:
Novel axonal projection from the caudal end of the ventrolateral medulla to the intermediolateral cell column
Homma I Developmental changes in the spatio-temporal pattern of respiratory neuron activity in the medulla of late fetal rat.
Homma I 晚期胎鼠髓质呼吸神经元活动时空模式的发育变化。
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Kulik;Akos;Ooashi N;Onimaru H
  • 通讯作者:
    Onimaru H
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ONIMARU Hiroshi其他文献

ONIMARU Hiroshi的其他文献

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{{ truncateString('ONIMARU Hiroshi', 18)}}的其他基金

Ionic mechanisms of CO2 sensitivity in Phox2b neurons as the medullary central chemoreceptor
作为髓质中枢化学感受器的 Phox2b 神经元 CO2 敏感性的离子机制
  • 批准号:
    22500296
  • 财政年份:
    2010
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Neuronal mechanisms for determination of basic respiratory cycle by dual rhythm generators in the medulla
延髓双节律发生器确定基本呼吸周期的神经机制
  • 批准号:
    19500277
  • 财政年份:
    2007
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Developmental mechanisms from tetal to neonatal type of respiratory center as a functional neuron network
从四肢到新生儿型呼吸中枢作为功能神经元网络的发育机制
  • 批准号:
    13680880
  • 财政年份:
    2001
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Neuronal mechanisms of development of respiratory neuron network in the late fetal stage of rat
大鼠胎儿晚期呼吸神经元网络发育的神经机制
  • 批准号:
    10680753
  • 财政年份:
    1998
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Analysis of ionic channels involved in burst generation of respiratory neurons in newborn rat medulla in vitro.
体外新生大鼠髓质呼吸神经元爆发性生成中涉及的离子通道分析。
  • 批准号:
    07680883
  • 财政年份:
    1995
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Analysis of ionic channels of medullary respiratory neurons by whole-cell patch-clamp recordings
通过全细胞膜片钳记录分析髓质呼吸神经元的离子通道
  • 批准号:
    05680707
  • 财政年份:
    1993
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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Radiocontrast Nephropathy: Redox Degradation Catalyst and Nitric Oxide Donor
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    8449038
  • 财政年份:
    2013
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Modeling Solute Transport and Urine Concentrating Mechanism in the Rat Kidney
模拟大鼠肾脏中的溶质转运和尿液浓缩机制
  • 批准号:
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Modeling Solute Transport and Urine Concentrating Mechanism in the Rat Kidney
模拟大鼠肾脏中的溶质转运和尿液浓缩机制
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Modeling Solute Transport and Urine Concentrating Mechanism in the Rat Kidney
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Modeling Solute Transport and Urine Concentrating Mechanism in the Rat Kidney
模拟大鼠肾脏中的溶质转运和尿液浓缩机制
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Mechanism for Reduced Adrenomedullary Epinephrine Release in Type 1 Diabetes
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Mechanism for Reduced Adrenomedullary Epinephrine Release in Type 1 Diabetes
1 型糖尿病肾上腺髓质肾上腺素释放减少的机制
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Involvement of medulla neurons and glia in migraine model rat with photophobia
畏光偏头痛模型大鼠髓质神经元和胶质细胞的参与
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