Mitochondrial involvement in post-tetanic potentiation of synaptic transmission
Mitochondrial involvement in post-tetanic potentiation of synaptic transmission
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DOI：
10.1016/s0896-6273(00)81248-9
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发表时间：
1997-03-01
期刊：
影响因子：
16.2
通讯作者：
Zucker, RS
中科院分区：
文献类型：
--
作者：
Tang, YG;Zucker, RS
强直后增强（Posttetanic potentiation，PTP）是强直刺激后突触前持续性[Ca ~（2+）]（i）引起的突触传递的一个重要方面。在螯虾神经肌肉接头处，线粒体Ca 2+摄取和释放的几种抑制剂（四苯基磷或TPP+，羰基氰间氯苯腙或CCCP，和钌红）阻断PTP和突触前残留[Ca 2 +]（i）的持续，而内质网（ER）Ca 2+泵抑制剂和释放通道激活剂（毒胡萝卜素，2，5-二-（叔丁基）-1，4-苯并氢醌或BHQ，和咖啡因）没有影响。PTP显然是由强直性积累的线粒体Ca 2+的缓慢流出引起的。
Posttetanic potentiation (PTP) is an essential aspect of synaptic transmission that arises from a persistent presynaptic [Ca2+](i) following tetanic stimulation. At crayfish neuromuscular junctions, several inhibitors of mitochondrial Ca2+ uptake and release (tetraphenylphosphonium or TPP+, carbonyl cyanide m-chlorophenylhydrazone or CCCP, and ruthenium red) blocked PTP and the persistence of presynaptic residual [Ca2+](i), while endoplasmic reticulum (ER) Ca2+ pump inhibitors and release channel activators (thapsigargin, 2,5-di-(tert-butyl)-1,4-benzohydroquinone or BHQ, and caffeine) had no effects. PTP apparently results from the slow efflux of tetanically accumulated mitochondrial Ca2+.