Miyagawa M, Minota S, Koketsu K
Brain Res. 1981 Nov 16;224(2):305-13. doi: 10.1016/0006-8993(81)90861-1.
In isolated bullfrog's sympathetic ganglia it was examined if the release of acetylcholine (ACh) from presynaptic nerve terminals was changed when postsynaptic ganglion cells were activated antidromically. The fast excitatory postsynaptic potential (fast EPSP) of ganglion cells was found to be depressed, whereas the nicotinic ACh potential of these cells was not depressed, immediately after these ganglion cells were activated by antidromic axonal or direct intracellular stimulations. This indicates that activation of ganglion cells results in inhibiton of the release of ACh from their presynaptic nerve terminals. Such an antidromic inhibition of ACh release could not be clearly observed when preparations were perfused with Ca2+-deficient solution or when adrenaline (10(-5) M) was added to the superfusion solution. Frequency of the spontaneous miniature EPSP was also found to be decreased after antidromic activation of ganglion cells. On the basis of these results it was concluded that some kind of transmitter was released from activated ganglion cells which inhibited ACh release by acting on preganglionic nerve terminals. This putative neurotransmitter was suggested to be adrenaline.
在离体牛蛙交感神经节中,研究了当逆向激活突触后神经节细胞时,突触前神经末梢乙酰胆碱(ACh)的释放是否发生变化。在通过逆向轴突刺激或直接细胞内刺激激活这些神经节细胞后,立即发现神经节细胞的快速兴奋性突触后电位(fast EPSP)受到抑制,而这些细胞的烟碱型ACh电位未受抑制。这表明神经节细胞的激活导致其突触前神经末梢ACh释放受到抑制。当用缺钙溶液灌注标本或在灌流液中加入肾上腺素(10⁻⁵ M)时,无法清楚观察到这种对ACh释放的逆向抑制。在逆向激活神经节细胞后,还发现自发微小EPSP的频率降低。基于这些结果得出结论,激活的神经节细胞释放某种递质,该递质通过作用于节前神经末梢来抑制ACh释放。这种假定的神经递质被认为是肾上腺素。