毒扁豆碱阻断了大鼠交感神经节神经元中的烟碱型乙酰胆碱受体。
Physostigmine blocked nicotinic acetylcholine receptors in rat sympathetic ganglion neurons.
作者信息
Zheng J Q, He X P, Yang A Z, Liu C G
机构信息
Institute of Pharmacology and Toxicology, Academy of Military Medical Sciences, Beijing, China.
出版信息
Zhongguo Yao Li Xue Bao. 1997 Nov;18(6):508-11.
AIM
To study the blocking mechanism of physostigmine (Phy) on nicotinic acetylcholine receptors (NAChR) in sympathetic neurons.
METHODS
The whole-cell patch-clamp technique was used to observe the effects of Phy on NAChR in the cultured sympathetic neurons from neonatal rat superior cervical ganglia (SCG).
RESULTS
Phy 5 -20 mumol.L-1 inhibited neuronal NAChR in a concentration-dependent manner and accelerated the desensitization of NAChR. Changing the membrane potential from -50 to -90 mV did not affect the blocking effect of Phy. Phy 200 mumol.L-1 did not induce any noticeable response in SCG neurons.
CONCLUSION
Phy blocked NAChR in the sympathetic ganglion neurons by interacting with the allosteric sites out of the binding sites and the open ionic channels of the receptors. Phy did not possess excitative effect on NAChR in SCG neurons.
目的
研究毒扁豆碱（Phy）对交感神经元烟碱型乙酰胆碱受体（NAChR）的阻断机制。
方法
采用全细胞膜片钳技术观察Phy对新生大鼠颈上神经节（SCG）培养的交感神经元中NAChR的影响。
结果
5 - 20μmol·L-1的Phy以浓度依赖的方式抑制神经元NAChR，并加速NAChR的脱敏。将膜电位从-50 mV改变为-90 mV不影响Phy的阻断作用。200μmol·L-1的Phy在SCG神经元中未诱导任何明显反应。
结论
Phy通过与受体结合位点和开放离子通道之外的变构位点相互作用来阻断交感神经节神经元中的NAChR。Phy对SCG神经元中的NAChR不具有兴奋作用。
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