氧化作为一种抑制性非上腺性非胆性神经递质
H Bult1, G E Boeckxstaens, P A Pelckmans
1Division of Pharmacology, Faculty of Medicine, University of Antwerp (UIA), Wilrijk, Belgium.
Nature
|May 24, 1990
概括
研究人员确定了氧化 (NO) 作为神经递质,由阻断性非上腺性非胆性 (NANC) 神经在犬类胆柱结节释放. 这一发现支持NO NO NO.
科学领域:
- 神经科学是一个神经科学.
- 胃肠病学 胃肠病学
- 药理学 药理学 是一个学科.
背景情况:
- 抑制性非上腺非胆性神经 (NANC) 在胃肠道调节中起着至关重要的作用.
- 负责NANC神经活动的特定神经递质仍然是争论的主题.
- 氧化 (NO) 被假设为潜在的NANC神经递质,但缺乏直接证据表明它在神经刺激时释放.
研究的目的:
- 为了研究由NANC神经释放的神经递质的身份,NANC神经在犬类大肠结节.
- 为释放氧化 (NO) 在刺激这些神经提供直接证据.
主要方法:
- 采用了超生物试验来检测从刺激的犬体大肠结NANC神经释放的血管松因子.
- 描述释放的因子的特性,包括组织选择性,化学稳定性和特定剂 (超氧化离子,血红蛋白) 的无活化.
- 评估了NG-nitro-L-arginine (L-NNA) 和L-arginine对该因子活性的影响.
主要成果:
- 在刺激犬类大肠结NANC神经时,证明了可转移的血管松因子的释放.
- 该因子的特征,包括其不稳定性,超氧化离子和血红蛋白的失活,以及L-NNA和L-阿尔金因的调节,与氧化 (NO) 一致.
- NG-nitro-L-arginine (L-NNA) 抑制了该因子的活性,而L-arginine则强化了它.
结论:
- 氧化 (NO) 被识别为由犬类胆管结节中的抑制性非上腺非胆管神经 (NANC) 释放的生物媒介.
- 这项研究提供了支持NO作为神经递质在胃肠道自主内化中的作用的直接证据.
- 这些发现有助于进一步了解NANC神经功能和肠道中神经传递.
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