Nordström O, Bartfai T
Acta Physiol Scand. 1980 Apr;108(4):347-53. doi: 10.1111/j.1748-1716.1980.tb06543.x.
Release of 3H-ACh from isolated nerve endings of rat hippocampus was evoked by incubation in Krebs-Ringer's buffer containing 25 or 35 mM potassium. The release was Ca2+-dependent and could be inhibited by Mg2+ (20 mM). The muscarinic antagonist, atropine (10(-10)-10(-6) M), enhanced 3H-ACh-release. The muscarinic agonist, carbachol (10(-5)-10(-3) M) inhibited 3H-ACh release via interaction with muscarinic receptors: this effect could be blocked by atropine (10(-6) M). The presence of the feed-back regulation of 3H-ACh release in a cell-free preparation provides further evidence that the presynaptic regulation is exerted by muscarinic autoreceptors localized on the cholinergic nerve ending itself. The feed back inhibition of the 3H-ACh release does not require the presence of intact neurons or neuronal loops as tetrodotoxin (2.5 x 10(-6) M) does not affect the above results.
在含有25或35 mM钾的Krebs - Ringer缓冲液中孵育可诱发大鼠海马离体神经末梢释放3H - ACh。这种释放依赖于Ca2 +,并可被Mg2 +(20 mM)抑制。毒蕈碱拮抗剂阿托品(10(-10)-10(-6) M)可增强3H - ACh的释放。毒蕈碱激动剂卡巴胆碱(10(-5)-10(-3) M)通过与毒蕈碱受体相互作用抑制3H - ACh释放:这种效应可被阿托品(10(-6) M)阻断。在无细胞制剂中存在3H - ACh释放的反馈调节,进一步证明了突触前调节是由位于胆碱能神经末梢自身的毒蕈碱自受体发挥作用的。3H - ACh释放的反馈抑制不需要完整的神经元或神经回路的存在,因为河豚毒素(2.5×10(-6) M)不影响上述结果。