一氧化氮通过对鳃曳动物摄食神经元的细胞内酸化作用增强环磷酸腺苷门控阳离子电流。
Nitric oxide potentiates cAMP-gated cation current by intracellular acidification in feeding neurons of pleurobranchaea.
机构信息
Department of Molecular and Integrative Physiology, University of Illinois, Urbana, Illinois 61801, USA.
出版信息
J Neurophysiol. 2010 Aug;104(2):742-5. doi: 10.1152/jn.00021.2010. Epub 2010 May 19.
A pH-sensitive cAMP-gated cation current (I(Na,cAMP)) is widely distributed in neurons of the feeding motor networks of gastropods. In the sea slug Pleurobranchaea this current is potentiated by nitric oxide (NO), which itself is produced by many feeding neurons. The action of NO is not dependent on either cGMP or cAMP signaling pathways. However, we found that NO potentiation of I(Na,cAMP) in the serotonergic metacerebral cells could be blocked by intracellular injection of MOPS buffer (pH 7.2). In neurons injected with the pH indicator BCECF, NO induced rapid intracellular acidification to several tenths of a pH unit. Intracellular pH has not previously been identified as a specific target of NO, but in this system NO modulation of I(Na,cAMP) via pH(i) may be an important regulator of the excitability of the feeding motor network.
一种 pH 敏感的环磷酸鸟苷门控阳离子电流（I(Na,cAMP)）广泛分布于腹足纲动物摄食运动网络的神经元中。在海蛞蝓 Pleurobranchaea 中，这种电流可被一氧化氮（NO）增强，而一氧化氮本身又可被许多摄食神经元产生。NO 的作用不依赖于环鸟苷酸（cGMP）或环磷酸腺苷（cAMP）信号通路。然而，我们发现，NO 可增强 5-羟色胺能的脑侧体细胞中的 I(Na,cAMP)，但这种增强可被 pH 值为 7.2 的 MOPS 缓冲液（MOPS buffer）所阻断。在 pH 指示剂 BCECF 注入的神经元中，NO 可诱导细胞内迅速酸化至几个 pH 单位。细胞内 pH 值以前尚未被确定为 NO 的特定靶点，但在该系统中，NO 通过 pH(i)对 I(Na,cAMP)的调节可能是摄食运动网络兴奋性的重要调节剂。
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