Regulatory role of gamma-aminobutyric acid (GABA) in catecholamine release from adrenal medulla

γ-氨基丁酸(GABA)对肾上腺髓质释放儿茶酚胺的调节作用

基本信息

  • 批准号:
    62570088
  • 负责人:
  • 金额:
    $ 0.38万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
  • 财政年份:
    1987
  • 资助国家:
    日本
  • 起止时间:
    1987 至 1988
  • 项目状态:
    已结题

项目摘要

We investigated the role of gamma-aminobutyric acid (GABA) in catecholamine (CA) release from adrenal medulla using a primary culture of bovine adrenal chromaffin cells. 1. GABA elicited CA release from monolayer cultures of bovine adrenal chromaffin cells, and facilitated acetylcholine (ACh)-evoked CA release via GABA receptor. Benzodiazepines and pentbarbital enhanced the action of GABA. 2. GABA caused an increase in ^<45>Ca uptake associated with CA release. Ach-induced ^<45>Ca uptake was additively enhanced by GABA, whereas veratridine (at low concentration)- evoked ^<45>Ca uptake was more than additively enhanced by GABA. 3. GABA-evoked ^<45>Ca uptake and CA release were modified by replacing extracellular C1^- by impermeable anion or sucrose in a time-related fashion: sudden replacement of extracellular C^- by sucrose enhanced GABA-evoked CA release whereas long-term treatment with low C1^- medium reduced GABA-evoked CA release and ^<45>Ca uptake. 4. GABA increased bis-oxonol fluorescence, reflecting a depolarization of chromaffin cells. Furthermore, GABA caused an increase in cytosolic Ca^<2+> ([Ca^<2+>]i), assessed by quin2. GABA-induced depolarization and rise of [Ca^<2+>]i were well correlated with ^<45>Ca uptake and CA release.Based on these results, we concluded that GABA causes an influx of Ca^<2+> through voltage- gated Ca^<2+> channels as a consequence of depolarization via C1^--dependent mechanism. This, in turn, elicited [Ca^<2+>]i rise leading to an exocytotic release of CA by GABA itself and to an facilitatory modulation by GABA of stimulation-evoked CA release.
采用牛肾上腺嗜铬细胞原代培养方法,研究了γ-氨基丁酸(GABA)对肾上腺髓质释放儿茶酚胺(CA)的影响。1.GABA可诱导单层培养的牛肾上腺嗜铬细胞释放CA,并通过GABA受体促进乙酰胆碱(ACh)诱导的CA释放。苯二氮卓类药物和戊巴比妥可增强GABA的作用。2.GABA可引起CA释放相关的钙摄取增加。ACh诱导的钙摄取可被GABA相加增强,而藜芦碱(低浓度)诱导的钙摄取则大于GABA的相加增强。3.GABA诱导的钙摄取和CA释放被非渗透阴离子或蔗糖以时间相关的方式替换到胞外:蔗糖突然取代胞外的C^-,增强了GABA诱导的CA释放,而长期低C1^处理则减少了GABA诱导的CA释放和钙摄取。4.GABA增强了双氧酚荧光,反映了嗜铬细胞的去极化。此外,GABA引起细胞内[Ca^&lt;2+&gt;([Ca^&lt;2+&gt;]i)增加,用qu2进行评估。GABA引起的去极化和[Ca^&lt;2+&gt;]i升高与钙摄取和钙释放密切相关。根据这些结果,我们认为GABA通过电压门控性钙通道引起钙内流,其去极化机制依赖于c1^。这反过来又引起[Ca^&lt;2+]i升高,导致GABA自身胞吐释放CA,并促进GABA对刺激诱导的CA释放的调节。

项目成果

期刊论文数量(4)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Shigeo Kitayama et al.: Naunyn-Schmiedeberg's Arch. Phrmacol.
Shigeo Kitayama 等人:Naunyn-Schmiedeberg 拱门。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
S.Kitayama et al.: "GABA receptor-mediated increase of cytosolic Ca^<2+> in isolated bovine adrenal chromaffin cells." Biochim.Biophys.Acta. (1990)
S.Kitayama等人:“分离的牛肾上腺嗜铬细胞中GABA受体介导的胞质Ca 2+ 增加。”
  • DOI:
  • 发表时间:
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  • 影响因子:
    0
  • 作者:
  • 通讯作者:
S. Kitayama, K. Morita, T. Dohi, and A. Tsujimoto: "Enhancement by GABA of the stimulation-evoked catecholamine release from cultured bovine adrenal chromaffin cells." Naunyn-Schmiedeberg's Arch. Pharmacol.
S. Kitayama、K. Morita、T. Dohi 和 A. Tsujimoto:“GABA 增强培养牛肾上腺嗜铬细胞中刺激诱发的儿茶酚胺释放。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
S. Kitayama, K. Morita, T. Dohi, and A. Tsujimoto: "GABAergic modulation of catecholamine release from cultured bovine adrenal chromaffin cells. Evidence for the involvement of Cl^--dependent Ca^<2+> entry." Naunyn-Schmiedeberg's Arch. Pharmacol.
S. Kitayama、K. Morita、T. Dohi 和 A. Tsujimoto:“培养的牛肾上腺嗜铬细胞中儿茶酚胺释放的 GABA 能调节。Cl^-依赖性 Ca^2 进入参与的证据。”
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  • 影响因子:
    0
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KITAYAMA Shigeo其他文献

KITAYAMA Shigeo的其他文献

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{{ truncateString('KITAYAMA Shigeo', 18)}}的其他基金

Regulated expression and functional modulation of norepinephrine transporter by isoform interaction
通过异构体相互作用调节去甲肾上腺素转运蛋白的表达和功能调节
  • 批准号:
    13680844
  • 财政年份:
    2001
  • 资助金额:
    $ 0.38万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Regulation of the functional expression of neurotransmitter transporters by their RNA processing
通过 RNA 加工调节神经递质转运蛋白的功能表达
  • 批准号:
    11680756
  • 财政年份:
    1999
  • 资助金额:
    $ 0.38万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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