Schmid H A
Max-Planck-Institute for Physiological and Clinical Research, Bad Nauheim, Federal Republic of Germany.
Amino Acids. 1998;14(1-3):113-9. doi: 10.1007/BF01345251.
Blood-borne angiotensin II (AngII) is known to mediate water-intake by its excitatory effect on neurons in the subfornical organ (SFO). Conversely, nitric oxide (NO) has exclusively inhibitory effects on rat SFO-neurons and on SFO-mediated water-intake. Extracellular and patch-clamp recordings from freshly dissociated rat SFO-neurons showed that glutamate activates AngII-sensitive SFO-neurons by opening ligand-gated cation channels. An immunocytochemical study showed that activation of glutamate receptors increased the concentration of the inhibitory second messenger cGMP in the SFO. A model is proposed suggesting that NO protects SFO-neurons from overexcitability by excitatory neurotransmitters.
众所周知,血源性血管紧张素II(AngII)通过对穹窿下器(SFO)中的神经元产生兴奋作用来介导水摄入。相反,一氧化氮(NO)对大鼠SFO神经元和SFO介导的水摄入具有唯一的抑制作用。对新鲜分离的大鼠SFO神经元进行的细胞外和膜片钳记录表明,谷氨酸通过打开配体门控阳离子通道来激活对AngII敏感的SFO神经元。一项免疫细胞化学研究表明,谷氨酸受体的激活会增加SFO中抑制性第二信使环磷酸鸟苷(cGMP)的浓度。提出了一个模型,表明NO可保护SFO神经元免受兴奋性神经递质的过度刺激。