线粒体在突触传递强直后增强中的作用。
Mitochondrial involvement in post-tetanic potentiation of synaptic transmission.
作者信息
Tang Y, Zucker R S
机构信息
Division of Neurobiology, University of California, Berkeley 94720-3200, USA.
出版信息
Neuron. 1997 Mar;18(3):483-91. doi: 10.1016/s0896-6273(00)81248-9.
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+.
强直后增强（PTP）是突触传递的一个重要方面，它源于强直刺激后突触前[Ca2+]i的持续存在。在小龙虾神经肌肉接头处，几种线粒体Ca2+摄取和释放抑制剂（四苯基鏻或TPP+、羰基氰化物间氯苯腙或CCCP以及钌红）阻断了PTP和突触前残余[Ca2+]i的持续性，而内质网（ER）Ca2+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-苯二酚或BHQ以及咖啡因）则没有作用。PTP显然是由强直积累的线粒体Ca2+的缓慢外流引起的。
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