ArticleThe Journal of general physiology2000
Functional coupling of Ca(2+) channels to ryanodine receptors at presynaptic terminals. Amplification of exocytosis and plasticity.
Article in The Journal of general physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 113 citations in OpenAlex.
- Acute mitochondrial dysfunction impairs neuromuscular transmission and contractility in mouse diaphragm: the protective potential of 25-hydroxycholesterol.Journal of physiology and biochemistry · 2026Article
- Spatially non-overlapping CaCell reports · 2023Article
- Review
- Roles and Sources of Calcium in Synaptic Exocytosis.Advances in neurobiology · 2023Article
- Single Amino Acid Changes in the Ryanodine Receptor in the Human Population Have EffectsFrontiers in genetics · 2020Article
- The Ever-Growing Puzzle of Asynchronous Release.Frontiers in cellular neuroscience · 2019Review
- Role of membrane cholesterol in spontaneous exocytosis at frog neuromuscular synapses: reactive oxygen species-calcium interplay.The Journal of physiology · 2014Article
- Molecular mechanisms for synchronous, asynchronous, and spontaneous neurotransmitter release.Annual review of physiology · 2014Review
- The number of components of enhancement contributing to short-term synaptic plasticity at the neuromuscular synapse during patterned nerve Stimulation progressively decreases as basal release probability is increased from low to normal levels by changing extracellular Ca2+.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Ca2+ dependence of the binomial parameters p and n at the mouse neuromuscular junction.Journal of neurophysiology · 2010Article
- Synaptic mitochondria in synaptic transmission and organization of vesicle pools in health and disease.Frontiers in synaptic 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
- Maturation and long-term hypoxia alters Ca2+-induced Ca2+ release in sheep cerebrovascular sympathetic neurons.Journal of applied physiology (Bethesda, Md. : 1985) · 2009Article
- Excitatory and inhibitory synaptic transmission is differentially influenced by two ortho-substituted polychlorinated biphenyls in the hippocampal slice preparation.Toxicology and applied pharmacology · 2009Article
- Advancing age alters the contribution of calcium release from smooth endoplasmic reticulum stores in superior cervical ganglion cells.The journals of gerontology. Series A, Biological sciences and medical sciences · 2009Article
- Use-dependent amplification of presynaptic Ca2+ signaling by axonal ryanodine receptors at the hippocampal mossy fiber synapse.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- 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
- Bioluminescence imaging of mitochondrial Ca2+ dynamics in soma and neurites of individual adult mouse sympathetic neurons.The Journal of physiology · 2007Article
- Calcium regulation in individual peripheral sensory nerve terminals of the rat.The Journal of physiology · 2007Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca(2+)-induced Ca(2+) release (CICR) enhances a variety of cellular Ca(2+) signaling and functions. How CICR affects impulse-evoked transmitter release is unknown. At frog motor nerve terminals, repetitive Ca(2+) entries slowly prime and subsequently activate the mechanism of CICR via ryanodine receptors and asynchronous exocytosis of transmitters. Further Ca(2+) entry inactivates the CICR mechanism and the absence of Ca(2+) entry for >1 min results in its slow depriming. We now report here that the activation of this unique CICR markedly enhances impulse-evoked exocytosis of transmitter. The conditioning nerve stimulation (10-20 Hz, 2-10 min) that primes the CICR mechanism produced the marked enhancement of the amplitude and quantal content of end-plate potentials (EPPs) that decayed double exponentially with time constants of 1.85 and 10 min. The enhancement was blocked by inhibitors of ryanodine receptors and was accompanied by a slight prolongation of the peak times of EPP and the end-plate currents estimated from deconvolution of EPP. The conditioning nerve stimulation also enhanced single impulse- and tetanus-induced rises in intracellular Ca(2+) in the terminals with little change in time course. There was no change in the rate of growth of the amplitudes of EPPs in a short train after the conditioning stimulation. On the other hand, the augmentation and potentiation of EPP were enhanced, and then decreased in parallel with changes in intraterminal Ca(2+) during repetition of tetani. The results suggest that ryanodine receptors exist close to voltage-gated Ca(2+) channels in the presynaptic terminals and amplify the impulse-evoked exocytosis and its plasticity via CICR after Ca(2+)-dependent priming.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.