ArticleThe Journal of general physiology1998
A Ca2+-induced Ca2+ release mechanism involved in asynchronous exocytosis at frog motor nerve terminals.
Article in The Journal of general physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 94 citations in OpenAlex.
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- L-type CaProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Differential behaviors of calcium-induced calcium release in one dimensional dendrite by Nernst-Planck equation, cable model and pure diffusion model.Cognitive neurodynamics · 2024Article
- Review
- The Putative Drosophila TMEM184B Ortholog Tmep Ensures Proper Locomotion by Restraining Ectopic Firing at the Neuromuscular Junction.Molecular neurobiology · 2022Article
- The Ever-Growing Puzzle of Asynchronous Release.Frontiers in cellular neuroscience · 2019Review
- Bax inhibiting peptide reduces apoptosis in neonatal rat hypoxic-ischemic brain damage.International journal of clinical and experimental pathology · 2015Article
- Molecular mechanisms for synchronous, asynchronous, and spontaneous neurotransmitter release.Annual review of physiology · 2014Review
- Role of intracellular calcium stores in hair-cell ribbon synapse.Frontiers in cellular neuroscience · 2014Review
- Synchronous and asynchronous modes of synaptic transmission utilize different calcium sources.eLife · 2013Article
- Ryanodine receptors selectively contribute to the formation of taste-evoked calcium signals in mouse taste cells.The European journal of neuroscience · 2010Article
- Presynaptic mitochondria in functionally different motor neurons exhibit similar affinities for Ca2+ but exert little influence as Ca2+ buffers at nerve firing rates in situ.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Individual calcium syntillas do not trigger spontaneous exocytosis from nerve terminals of the neurohypophysis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Calcium release via activation of presynaptic IP3 receptors contributes to kainate-induced IPSC facilitation in rat neocortex.Neuropharmacology · 2008Article
- Perinatal exposure to a noncoplanar polychlorinated biphenyl alters tonotopy, receptive fields, and plasticity in rat primary auditory cortex.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Stimulation-induced changes in NADH fluorescence and mitochondrial membrane potential in lizard motor nerve terminals.The Journal of physiology · 2007Article
- Noradrenaline triggers multivesicular release at glutamatergic synapses in the hypothalamus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Ca2+ sparks and secretion in dorsal root ganglion neurons.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Presynaptic ryanodine receptors are required for normal quantal size at the Caenorhabditis elegans neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extent to which Ca2+-induced Ca2+ release (CICR) affects transmitter release is unknown. Continuous nerve stimulation (20-50 Hz) caused slow transient increases in miniature end-plate potential (MEPP) frequency (MEPP-hump) and intracellular free Ca2+ ([Ca2+]i) in presynaptic terminals (Ca2+-hump) in frog skeletal muscles over a period of minutes in a low Ca2+, high Mg2+ solution. Mn2+ quenched Indo-1 and Fura-2 fluorescence, thus indicating that stimulation was accompanied by opening of voltage-dependent Ca2+ channels. MEPP-hump depended on extracellular Ca2+ (0.05-0.2 mM) and stimulation frequency. Both the Ca2+- and MEPP-humps were blocked by 8-(N, N-diethylamino)octyl3,4,5-trimethoxybenzoate hydrochloride (TMB-8), ryanodine, and thapsigargin, but enhanced by CN-. Thus, Ca2+-hump is generated by the activation of CICR via ryanodine receptors by Ca2+ entry, producing MEPP-hump. A short interruption of tetanus (<1 min) during MEPP-hump quickly reduced MEPP frequency to a level attained under the effect of TMB-8 or thapsigargin, while resuming tetanus swiftly raised MEPP frequency to the previous or higher level. Thus, the steady/equilibrium condition balancing CICR and Ca2+ clearance occurs in nerve terminals with slow changes toward a greater activation of CICR (priming) during the rising phase of MEPP-hump and toward a smaller activation during the decay phase. A short pause applied after the end of MEPP- or Ca2+-hump affected little MEPP frequency or [Ca2+]i, but caused a quick increase (faster than MEPP- or Ca2+-hump) after the pause, whose magnitude increased with an increase in pause duration (<1 min), suggesting that Ca2+ entry-dependent inactivation, but not depriming process, explains the decay of the humps. The depriming process was seen by giving a much longer pause (>1 min). Thus, ryanodine receptors in frog motor nerve terminals are endowed with Ca2+ entry-dependent slow priming and fast inactivation mechanisms, as well as Ca2+ entry-dependent activation, and involved in asynchronous exocytosis. Physiological significance of CICR in presynaptic terminals was discussed.
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