Mitochondrial involvement in post-tetanic potentiation of synaptic transmission.
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+.
Tang
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Division of Neurobiology, University of California, Berkeley 94720-3200, USA.
Zucker
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RS
D000818:Animals; D003400:Astacoidea / Q000502:physiology; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone / Q000494:pharmacology; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology*; D009119:Muscle Contraction / Q000502:physiology*; D009469:Neuromuscular Junction / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D009861:Onium Compounds / Q000494:pharmacology*; D009943:Organophosphorus Compounds / Q000494:pharmacology*; D010085:Oxidative Phosphorylation / Q000187:drug effects; D012430:Ruthenium Red / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D019284:Thapsigargin / Q000494:pharmacology; D014475:Uncoupling Agents / Q000494:pharmacology
D009861:Onium Compounds; D009943:Organophosphorus Compounds; D014475:Uncoupling Agents; D012430:Ruthenium Red; D002110:Caffeine; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone; D019284:Thapsigargin; D002118:Calcium; C013289:tetraphenylphosphonium