A note of the mechanism by which inhibitors of the sodium pump accelerate spontaneous release of transmitter from motor nerve terminals.
A note of the mechanism by which inhibitors of the sodium pump accelerate spontaneous release of transmitter from motor nerve terminals.
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关于钠泵抑制剂加速运动神经末梢自发释放递质的机制的说明。
DOI：
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发表时间：
1975
期刊：
影响因子：
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通讯作者：
A. Crawford
中科院分区：
文献类型：
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作者：
P. F. Baker;A. Crawford
1. 0-1 mM 哇巴因和无钾林格氏液在青蛙神经肌肉接头处的作用已被检查。 2. 延迟超过 30 分钟后，哇巴因会导致微型终板电位 (m.e.p.p.) 频率增加。这种增加在含有 1 mM-EGTA 的无 Ca 林格氏液中没有发生变化，因此不太可能是由于 Ca 进入运动神经末梢所致。 3. 如果在含有 0-1 mM 哇巴因和 1 mM-EGTA 的无钙林格氏液中重复刺激制剂的神经，则 m.e.p.p. 的反应会降低。频率取决于破伤风相对于哇巴因治疗开始的时间。 4. 在接触哇巴因的前 30 分钟内，破伤风会导致 m.e.p.p 出现小幅短暂增加。频率与哇巴因出现之前发生的频率相似。大约 30 分钟后，相同的破伤风会导致 m.e.p.p 大幅且不可逆地增加。频率。 5. 将无 K 林格液注入终板会导致 m.e.p.p 立即呈指数上升。频率不受外部 Ca 离子存在的影响。更换振铃器 (2 mM) 的正常 K 后，m.e.p.p.频率很快恢复到原来的值。 6. 晚期暴露于 0-1 mM 哇巴因 m.e.p.p.频率对外部 Na 浓度 [Na]o 的变化变得极其敏感。减少 [Na]o 会增加 m.e.p.p.频率。对 [Na]o 的敏感性与外部 Ca 离子或 NaCl 的等渗替代物是 LiCl 还是蔗糖无关。 7. 有人认为，通过阻断 Na-K 交换泵而导致神经末梢单价阳离子含量的变化，在某种程度上促进了递质的自发释放。 m.e.p.p 的 Na 敏感性如果突触前末梢膜中存在 Na 依赖的 Ca 外流系统，则可以解释同时发生的频率。
1. The actions of 0–1 mM ouabain and of K‐free Ringer have been examined at the frog neuromuscular junction. 2. After a delay of more than 30 min, ouabain produces an increase in the miniature end‐plate potential (m.e.p.p.) frequency. This increase occurs unchanged in Ca‐free Ringer containing 1 mM‐EGTA and is therefore unlikely to be due to an entry of Ca into the motor nerve terminals. 3. If the nerve to the preparation is stimulated repetitively in Ca‐free Ringer containing 0–1 mM ouabain and 1 mM‐EGTA the response of the m.e.p.p. frequency depends on the timing of the tetanus relative to the beginning of the ouabain treatment. 4. During the first 30 min of exposure to ouabain, the tetanus produces a small, transient increase in the m.e.p.p. frequency similar to that which occurs before ouabain is present. After about 30 min the same tetanus produces large, irreversible increases in the m.e.p.p. frequency. 5. Superfusion of an end‐plate with K‐free Ringer causes an immediate exponential rise in the m.e.p.p. frequency that is unaffected by the presence of external Ca ions. On replacing the normal K of the Ringer (2 mM) the m.e.p.p. frequency recovers quickly to its original value. 6. Late in an exposure to 0–1 mM ouabain the m.e.p.p. frequency becomes extremely sensitive to changes in the external Na concentration, [Na]o. Reducing [Na]o increases the m.e.p.p. frequency. The sensitivity to [Na]o is independent of external Ca ions or whether the isotonic substitute for NaCl is LiCl or sucrose. 7. It is suggested that the spontaneous release of transmitter is facilitated, in some way, by the changes in the monovalent cation content of the nerve terminals that result from blocking the Na‐K exchange pump. The Na sensitivity of the m.e.p.p. frequency that develops simultaneously can be explained if a Na‐dependent Ca efflux system is present in the membrane of the presynaptic terminals.