ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Dihydropyridine receptors and type 1 ryanodine receptors constitute the molecular machinery for voltage-induced Ca2+ release in nerve terminals.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 57 citations in OpenAlex.
- The diverse forms and roles of the neuronal endoplasmic reticulum.Nature reviews. Neuroscience · 2026Review
- RyR1-mediated CaProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Voltage-induced calcium release inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Roles and Sources of Calcium in Synaptic Exocytosis.Advances in neurobiology · 2023Article
- Non-canonical Molecular Targets for Novel Analgesics: Intracellular Calcium and HCN Channels.Current neuropharmacology · 2021Review
- Advances in the neurophysiology of magnocellular neuroendocrine cells.Journal of neuroendocrinology · 2020Review
- Depolarizing, inhibitory GABA type A receptor activity regulates GABAergic synapse plasticity via ERK and BDNF signaling.Neuropharmacology · 2018Article
- Distinct Components of Retrograde Ca(V)1.1-RyR1 Coupling Revealed by a Lethal Mutation in RyR1.Biophysical journal · 2016Article
- Article
- Catecholamine exocytosis during low frequency stimulation in mouse adrenal chromaffin cells is primarily asynchronous and controlled by the novel mechanism of Ca2+ syntilla suppression.The Journal of physiology · 2014Article
- Functional ryanodine receptors in the membranes of neurohypophysial secretory granules.The Journal of general physiology · 2014Article
- μ-Opioid inhibition of Ca2+ currents and secretion in isolated terminals of the neurohypophysis occurs via ryanodine-sensitive Ca2+ stores.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- In-VITRo effect of Ficus deltoidea on the contraction of isolated rat's uteri is mediated via multiple receptors binding and is dependent on extracellular calcium.BMC complementary and alternative medicine · 2013Article
- Ca(V)1.1: The atypical prototypical voltage-gated Ca²⁺ channel.Biochimica et biophysica acta · 2013Review
- Ryanodine Receptors Selectively Interact with L Type Calcium Channels in Mouse Taste Cells.PloS one · 2013Article
- Type 1 ryanodine receptor knock-in mutation causing central core disease of skeletal muscle also displays a neuronal phenotype.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Somatic depolarization enhances GABA release in cerebellar interneurons via a calcium/protein kinase C pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity.Pharmacology & therapeutics · 2010Review
- Ionic conditions modulate stimulus-induced capacitance changes in isolated neurohypophysial terminals of the rat.The Journal of physiology · 2010Article
- Homer and the ryanodine receptor.European biophysics journal : EBJ · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Ca2+ stores were studied in a preparation of freshly dissociated terminals from hypothalamic magnocellular neurons. Depolarization from a holding level of -80 mV in the absence of extracellular Ca2+ elicited Ca2+ release from intraterminal stores, a ryanodine-sensitive process designated as voltage-induced Ca2+ release (VICaR). The release took one of two forms: an increase in the frequency but not the quantal size of Ca2+ syntillas, which are brief, focal Ca2+ transients, or an increase in global [Ca2+]. The present study provides evidence that the sensors of membrane potential for VICaR are dihydropyridine receptors (DHPRs). First, over the range of -80 to -60 mV, in which there was no detectable voltage-gated inward Ca2+ current, syntilla frequency was increased e-fold per 8.4 mV of depolarization, a value consistent with the voltage sensitivity of DHPR-mediated VICaR in skeletal muscle. Second, VICaR was blocked by the dihydropyridine antagonist nifedipine, which immobilizes the gating charge of DHPRs but not by Cd2+ or FPL 64176 (methyl 2,5 dimethyl-4[2-(phenylmethyl)benzoyl]-1H-pyrrole-3-carboxylate), a non-dihydropyridine agonist specific for L-type Ca2+ channels, having no effect on gating charge movement. At 0 mV, the IC50 for nifedipine blockade of VICaR in the form of syntillas was 214 nM in the absence of extracellular Ca2+. Third, type 1 ryanodine receptors, the type to which DHPRs are coupled in skeletal muscle, were detected immunohistochemically at the plasma membrane of the terminals. VICaR may constitute a new link between neuronal activity, as signaled by depolarization, and a rise in intraterminal Ca2+.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.