Abstract
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+.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Astacoidea / physiology
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Caffeine / pharmacology
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Calcium / metabolism
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Carbonyl Cyanide m-Chlorophenyl Hydrazone / pharmacology
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Endoplasmic Reticulum / drug effects
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Endoplasmic Reticulum / metabolism
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Mitochondria / drug effects
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Mitochondria / physiology*
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Muscle Contraction / physiology*
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Neuromuscular Junction / physiology*
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Neuronal Plasticity / physiology*
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Onium Compounds / pharmacology*
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Organophosphorus Compounds / pharmacology*
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Oxidative Phosphorylation / drug effects
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Ruthenium Red / pharmacology
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology*
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Thapsigargin / pharmacology
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Uncoupling Agents / pharmacology
Substances
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Onium Compounds
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Organophosphorus Compounds
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Uncoupling Agents
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Ruthenium Red
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Caffeine
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Carbonyl Cyanide m-Chlorophenyl Hydrazone
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Thapsigargin
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Calcium
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tetraphenylphosphonium