Edwards C, Dolezal V, Tucek S, Zemkova H, Vyskocil F
Institute of Physiology, Czechoslovak Academy of Science, Prague.
P R Health Sci J. 1988 Aug;7(2):71-4.
The effects on the spontaneous, non-quantal release of acetylcholine (ACh) from motor nerve terminals of substances known to inhibit the ACh transport system present in cholinergic synaptic vesicles have been investigated. In mouse diaphragms, the hyperpolarization normally produced by d-tubocurarine (dTC) in muscle endplates that had been treated by an anticholinesterase was partly or completely abolished by 2-(4-phenylpiperidino) cyclohexanol (AH5183, 10(-7)-10(-6)M), quinacrine (10(-7)M) and tetraphenylborate (10(-6) M). Since the sensitivity of the endplate to ACh was not changed, the block of the dTC induced hyperpolarization indicated an inhibition of the spontaneous, non-quantal release of ACh. This was confirmed by direct measurement of the ACh released by rat diaphragm. The release of ACh from the innervated diaphragm was decreased by about 50% by AH5183 (10(-8)-10(-6) M) and by 42% by quinacrine (10(-7)-10(-6) M). The ACh released was presumably neural, since the release of ACh from 4-day denervated diaphragms was not diminished by either AH5183 or quinacrine. The results indicate that the spontaneous release of ACh from the motor nerve terminals is probably mediated by a carrier which may be the vesicular transport system responsible for moving ACh into the vesicle. The transport system is likely incorporated into the membrane of the nerve terminal during exocytosis.
已知某些物质可抑制胆碱能突触小泡中存在的乙酰胆碱（ACh）转运系统，我们对其对运动神经末梢乙酰胆碱自发、非量子性释放的影响进行了研究。在小鼠膈神经-膈肌标本中，用抗胆碱酯酶处理过的肌肉终板，正常情况下由d-筒箭毒碱（dTC）产生的超极化，会被2-（4-苯基哌啶基）环己醇（AH5183，10⁻⁷ - 10⁻⁶M）、奎纳克林（10⁻⁷M）和四苯硼酸盐（10⁻⁶M）部分或完全消除。由于终板对ACh的敏感性未改变，dTC诱导的超极化受阻表明ACh的自发、非量子性释放受到抑制。这一点通过直接测量大鼠膈神经-膈肌标本释放的ACh得到了证实。AH5183（10⁻⁸ - 10⁻⁶M）使受神经支配的膈肌释放的ACh减少约50%，奎纳克林（10⁻⁷ - 10⁻⁶M）使其减少42%。释放的ACh大概来自神经，因为AH5183或奎纳克林都不会使去神经支配4天的膈肌释放的ACh减少。结果表明，运动神经末梢ACh的自发释放可能由一种载体介导，该载体可能是负责将ACh转运到小泡中的小泡转运系统。该转运系统可能在胞吐过程中整合到神经末梢的膜中。
