ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Ca2+- and voltage-dependent inactivation of Ca2+ channels in nerve terminals of the neurohypophysis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 54 citations in OpenAlex.
- Mathematical modelling of the oxytocin and vasopressin secretory system.Current opinion in endocrine and metabolic research · 2022Review
- Coupling of SK channels, L-type CaScientific reports · 2018Article
- Multiple cytosolic calcium buffers in posterior pituitary nerve terminals.The Journal of general physiology · 2016Article
- Ca(2+) current facilitation determines short-term facilitation at inhibitory synapses between cerebellar Purkinje cells.The Journal of physiology · 2015Article
- Article
- Calmodulin regulation (calmodulation) of voltage-gated calcium channels.The Journal of general physiology · 2014Review
- 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
- Spike triggered hormone secretion in vasopressin cells; a model investigation of mechanism and heterogeneous population function.PLoS computational biology · 2013Article
- Localized calcineurin confers Ca2+-dependent inactivation on neuronal L-type Ca2+ channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Ca2+-dependent modulation of voltage-gated Ca2+ channels.Biochimica et biophysica acta · 2012Review
- Voltage-gated calcium channels.Cold Spring Harbor perspectives in biology · 2011Review
- Modulation of calcium-dependent inactivation of L-type Ca2+ channels via β-adrenergic signaling in thalamocortical relay neurons.PloS one · 2011Article
- Signaling complexes of voltage-gated sodium and calcium channels.Neuroscience letters · 2010Review
- Hippocampal 'zipper' slice studies reveal a necessary role for calcineurin in the increased activity of L-type Ca(2+) channels with aging.Neurobiology of aging · 2010Article
- A mutation in the first intracellular loop of CACNA1A prevents P/Q channel modulation by SNARE proteins and lowers exocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- The hemiplegic migraine-associated Y1245C mutation in CACNA1A results in a gain of channel function due to its effect on the voltage sensor and G-protein-mediated inhibition.Pflugers Archiv : European journal of physiology · 2009Article
- Functional roles of cytoplasmic loops and pore lining transmembrane helices in the voltage-dependent inactivation of HVA calcium channels.The Journal of physiology · 2004Review
- Activity-dependent depression of excitability and calcium transients in the neurohypophysis suggests a model of "stuttering conduction".The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Calcineurin enhances L-type Ca(2+) channel activity in hippocampal neurons: increased effect with age in culture.Neuroscience · 2002Article
- Dependence of transient and residual calcium dynamics on action-potential patterning during neuropeptide secretion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Ca2+ channel inactivation was investigated in neurohypophysial nerve terminals by using patch-clamp techniques. The contribution of intracellular Ca2+ to inactivation was evaluated by replacing Ca2+ with Ba2+ or by including BAPTA in the internal recording solution. Ca2+ channel inactivation during depolarizing pulses was primarily voltage-dependent. A contribution of intracellular Ca2+ was revealed by comparing steady-state inactivation of Ca2+ channels with Ca2+ current and with intracellular [Ca2+]. However, this contribution was small compared to that of voltage. In contrast to voltage-gated Ca2+ channels in other preparations, in the neurohypophysis Ba2+ substitution or intracellular BAPTA increased the speed of inactivation while reducing the steady-state level of inactivation. Ca2+ channel recovery from inactivation was studied by using a paired-pulse protocol. The rate of Ca2+ channel recovery from inactivation at negative potentials was increased dramatically by Ba2+ substitution or intracellular BAPTA, indicating that intracellular Ca2+ inhibits recovery. Stimulation with trains of brief pulses designed to mimic physiological bursts of electrical activity showed that Ca2+ channel inactivation was much greater with 20 Hz trains than with 14 Hz trains. Inactivation induced by 20 Hz trains was reduced by intracellular BAPTA, suggesting an important role for Ca2+-dependent inactivation during physiologically relevant forms of electrical activity. Inhibitors of calmodulin and calcineurin had no effect on Ca2+ channel inactivation, arguing against a mechanism of inactivation involving these Ca2+-dependent proteins. The inactivation behavior described here, in which voltage effects on Ca2+ channel inactivation predominate at positive potentials and Ca2+ effects predominate at negative potentials, may be relevant to the regulation of neuropeptide release.
Indexed as
Identifiers
9221775PMC6573212W2138326703What 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.