Tan W, Du C, Siegelbaum S A, Role L W
Department of Anatomy and Cell Biology, Center for Neurobiology and Behavior, Howard Hughes Medical Institute, Columbia University, New York, New York 10032, USA.
J Neurophysiol. 1998 Feb;79(2):870-8. doi: 10.1152/jn.1998.79.2.870.
The effects of prostaglandin E2 (PGE2), an important metabolite of arachidonic acid, were studied on the activity of nicotinic AChR channels in cultured chick sympathetic ganglion neurons. In whole cell recordings, PGE2 (25 nM) inhibited significantly the ACh-evoked macroscopic current. In cell-attached patch recordings, PGE2 significantly inhibited single AChR channel currents as a result of a decrease in the frequency of channel opening, with no change in open time and conductance. PGE2 did not alter the extent or rate of agonist-induced desensitization of the AChR channels. These effects are specific since the related compound PGD2 had no effect on AChR channel function. Because there is an abundant endogenous production of PGE2 within sympathetic ganglia in response to certain stimuli, the inhibition of AChR channel function by PGE2 could serve an important role to modulate synaptic transmission in the sympathetic nervous system.
花生四烯酸的一种重要代谢产物前列腺素E2（PGE2）对培养的鸡交感神经节神经元中烟碱型乙酰胆碱受体（AChR）通道活性的影响进行了研究。在全细胞记录中，PGE2（25 nM）显著抑制了乙酰胆碱（ACh）诱发的宏观电流。在细胞贴附式膜片钳记录中，PGE2由于通道开放频率降低而显著抑制单个AChR通道电流，开放时间和电导无变化。PGE2没有改变激动剂诱导的AChR通道脱敏的程度或速率。这些效应是特异性的，因为相关化合物前列腺素D2（PGD2）对AChR通道功能没有影响。由于交感神经节内对某些刺激有丰富的内源性PGE2产生，PGE2对AChR通道功能的抑制可能在调节交感神经系统的突触传递中起重要作用。
