Analysis of nociceptive system in pathologic conditions

病理条件下伤害感受系统分析

基本信息

  • 批准号:
    06044255
  • 负责人:
  • 金额:
    --
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Overseas Scientific Survey.
  • 财政年份:
    1994
  • 资助国家:
    日本
  • 起止时间:
    1994 至 无数据
  • 项目状态:
    已结题

项目摘要

The polymodal receptor, one of the peripheral pain receptors, is involved in acute and chronic inflammatory pain. Its excitability is able to be modified by inflammation-related substances, changes in tissue temperature, etc. Under acute or chronic inflammatory processes, inflammatory mediators such as BK,PGs, 5-HT are suggested to be released in inflammatory region. So far, it has been impossible to record receptor activities from free nerve endings because of their small size. At present we have a good possibility to clarify the mechanisms of action of mediators on nociceptor membrane or intracellular dynamics using intracellular recording and patch clamp techniques from dorsal root ganglion cells (DRG cells), since we have demonstrated that the membrane characteristics and sensitivity to capsaicin (CAP) of DRG cells are closely resemble those of receptor membrane.In this project we clarified the effect of BK (10muM) on cultured DRG cells from intact rat, using of neurophysiological techniques. The results are followed :(1) In cultured cell within 24 hr.with and without NGF,the BK did not affect membrane potential, membrane input resistance and membrane current of CAP-sensitive cells.(2) Cultured CAP-sensitive cells more than 48 hr.were depolarized by the BK with action potentials. In the cultured cells with NGF the depolarization by the BK were much bigger than one of cultured cells without NGF.For next steps, we will observe PGs and 5-HT effects on cultured DRG cells and they will be compared with results obtained from rats under acute or chronic pathological conditions.
多模态受体是外周疼痛受体之一,参与急性和慢性炎症性疼痛。它的兴奋性可以被炎症相关物质、组织温度的变化等所改变。在急性或慢性炎症过程中,炎症介质如BK、PGs、5-HT被认为在炎症区域释放。到目前为止,由于自由神经末梢的体积小,还不可能记录它们的受体活动。目前,我们很有可能利用背根神经节细胞(DRG细胞)的细胞内记录和膜片钳技术来阐明介质对伤害感受器膜或细胞内动力学的作用机制,因为我们已经证明DRG细胞的膜特性和对辣椒素(CAP)的敏感性与受体膜非常相似。在本项目中,我们利用神经生理学技术阐明了BK (10muM)对培养的完整大鼠DRG细胞的影响。结果如下:(1)培养细胞24h内。不论有无NGF, BK均不影响cap敏感细胞的膜电位、膜输入电阻和膜电流。(2) cap敏感细胞培养超过48小时。被BK动作电位去极化。在有NGF的细胞中,BK的去极化作用明显大于无NGF的细胞。下一步,我们将观察pg和5-HT对培养DRG细胞的影响,并将其与急性或慢性病理状态下大鼠的结果进行比较。

项目成果

期刊论文数量(18)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
MIZUMURA Kazue,MINAGAWA Munenori,KODA Hisashi,KUMAZAWA Takao: "Forskolin does not augment the bradykinin response of canine visceral polymodal receptors in vitro." Neuroscience Letters. 166. 195-198 (1994)
MIZUMURA​​ Kazue、MINAGAWA Munenori、KODA Hisashi、KUMAZAWA Takao:“Forskolin 不会在体外增强犬内脏多模式受体的缓激肽反应。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
MIZUMURA Kazue, MINAGAWA Munenori, KODA Hisashi, KUMAZAWA Takao: "Histamine-induced sensitization of the heat response of canine visceral polymodal receptors." Neuroscience Letters. 168. 93-96 (1994)
MIZUMURA​​ Kazue、MINAGAWA Munenori、KODA Hisashi、KUMAZAWA Takao:“组胺诱导的犬内脏多模式受体热反应致敏。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
SATO Jun,SUZUKI Shigeyuki,TAMURA Ryoko,KUMAZAWA Takao: "Norepinephrine excitation of cutaneous nociceptorsin adjuvant-induced inflamed rats does not depend on sympathetic neurons." Neuroscience Letters. 177. 135-138 (1994)
SATO Jun、SUZUKI Shigeyuki、TAMURA Ryoko、KUMAZAWA Takao:“佐剂诱导的炎症大鼠皮肤伤害感受器的去甲肾上腺素兴奋不依赖于交感神经元。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
KUMAZAWA Takao: "Neurobiology of Nociceptors." Oxford Univ.Press(in press),
熊泽隆雄:“伤害感受器的神经生物学”。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
MIZUMURA Kazue,MINAGAWA Munenori,KODA Hisashi,KUMAZAWA Takao: "Histamine-induced sensitization of the heat response of canine visceral Polymodal receptors." Neuroscience Letters. 168. 93-96 (1994)
MIZUMURA​​ Kazue、MINAGAWA Munenori、KODA Hisashi、KUMAZAWA Takao:“组胺诱导的犬内脏多模式受体热反应致敏。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
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KUMAZAWA Takao其他文献

KUMAZAWA Takao的其他文献

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{{ truncateString('KUMAZAWA Takao', 18)}}的其他基金

Development of nonstationary point process model of swarm activity for monitoring of volcanic activity and aseismic slip
开发用于监测火山活动和地震滑移的群体活动非平稳点过程模型
  • 批准号:
    16K00065
  • 财政年份:
    2016
  • 资助金额:
    --
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Systemic and molecular analysis on the pathology of newly-developed myopathic chronic pain models
新开发的肌病性慢性疼痛模型病理学的系统和分子分析
  • 批准号:
    18613020
  • 财政年份:
    2006
  • 资助金额:
    --
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Analysis of nociceptive system in pathologic conditions
病理条件下伤害感受系统分析
  • 批准号:
    07044318
  • 财政年份:
    1995
  • 资助金额:
    --
  • 项目类别:
    Grant-in-Aid for International Scientific Research.
Physiological and Morphological Studies on Characteristics of Nociceptive Primary Afferent Neurons (Polymodal Receptors).
伤害性初级传入神经元(多模式受体)特征的生理学和形态学研究。
  • 批准号:
    01480122
  • 财政年份:
    1989
  • 资助金额:
    --
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)
Development of expiratory CO2-concentration control system for regulation of autonomic nervous tone by the adaptive control method.
开发呼气二氧化碳浓度控制系统,通过自适应控制方法调节自主神经张力。
  • 批准号:
    61870006
  • 财政年份:
    1986
  • 资助金额:
    --
  • 项目类别:
    Grant-in-Aid for Developmental Scientific Research
Neuro-humoral mechanisms of relexive respiratory suppression mediated by endogenous opiated system.
内源性阿片系统介导的反射性呼吸抑制的神经体液机制。
  • 批准号:
    60440027
  • 财政年份:
    1985
  • 资助金额:
    --
  • 项目类别:
    Grant-in-Aid for General Scientific Research (A)

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