Mitochondrial Involvement in Post-Tetanic Potentiation of Synaptic Transmission
1997; Cell Press; Volume: 18; Issue: 3 Linguagem: Inglês
10.1016/s0896-6273(00)81248-9
ISSN1097-4199
AutoresYun-gui Tang, Robert S. Zucker,
Tópico(s)Mitochondrial Function and Pathology
ResumoPosttetanic 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+.
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