On the association between transmitter secretion and the release of adenine nucleotides from mammalian motor nerve terminals.
On the association between transmitter secretion and the release of adenine nucleotides from mammalian motor nerve terminals.
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关于递质分泌与哺乳动物运动神经末梢释放腺嘌呤核苷酸之间的关联。
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发表时间：
1975
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通讯作者：
E. M. Silinsky
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作者：
E. M. Silinsky
1.使用常规电生理技术记录离体大鼠膈神经-半膈制备物。在休息（20分钟）或神经刺激（7次/秒，20分钟）后，除去制备物的浸浴介质，并使用萤火虫荧光素酶方法的灵敏修改（Silinsky，1974）测定三磷酸腺苷（ATP）和二磷酸腺苷（ADP）。2.在筒箭毒碱和正常（2 mM）钙的存在下，14个神经刺激周期（8种制剂）引起ATP和/或ADP的出现，其量范围为28至641 p-mole。使用卡巴胆碱（30 μ M或1 mM）的实验表明，这种核苷酸流出不是由释放的乙酰胆碱（ACh）的次级作用产生的。3.以7次/秒的速度刺激膈神经干20分钟，不引起ATP或ADP的外排。4.在正常渗透压和钙浓度降低（0-1 mM或“无钙”）的溶液中，刺激无法从非收缩制剂中释放腺嘌呤核苷酸。5.将膈肌浸泡在正常钙中，并在5倍10 - 5 M半胆碱-3的存在下以11/sec间接刺激80-90 min。在所有可检测到的ACh释放迹象被消除后，神经刺激未能释放ATP或ADP。6.这些结果与外源性ATP水解的实验相结合，表明ATP从运动神经末梢释放，随后通过酶活性降解。也有人建议，释放的核苷酸可能来自胆碱能囊泡。
1. Conventional electrophysiological techniques were used to record from isolated rat phrenic nerve‐hemidiaphragm preparations. After periods of rest (20 min) or nerve stimulation (7/sec for 20 min) the bathing medium of the preparation was removed and assayed for adenosine triphosphate (ATP) and adenosine diphosphate (ADP) using a sensitive modification of the firefly luciferase method (Silinsky, 1974). 2. In the presence of tubocurarine and normal (2 mM) calcium, fourteen periods of nerve stimulation (eight preparations) caused the appearance of ATP and/or ADP in amounts ranging from 28 to 641 p‐mole. Experiments using carbachol (30 muM or 1 mM) suggested that this nucleotide efflux was not produced by a secondary action of released acetylcholine (ACh). 3. Stimulation of isolate phrenic nerve trunks at 7/sec for 20 min did not cause the efflux of ATP or ADP. 4. In solutions of normal osmotic pressure and reduced calcium concentrations (0–1 mM or ‘calcium‐free’), stimulation failed to release adenine nucleotide from non‐contracting preparations. 5. Diaphragms were bathed in normal calcium and indirectly stimulated at 11/sec for 80–90 min in the presence of 5 times 10‐minus 5 M hemicholinium‐3. After all detectable signs of ACh release were eliminated, nerve stimulation failed to release ATP or ADP. 6. These results in conjunction with experiments on the hydrolysis of exogenous ATP suggest that ATP is released from the motor nerve ending and is subsequently degraded by enzymatic activity. It is also suggested that the released nucleotide may be derived from the cholinergic vesicle.