Evidence map›Paper›PMID 9295386›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997

All-or-none Ca2+ release from intracellular stores triggered by Ca2+ influx through voltage-gated Ca2+ channels in rat sensory neurons.

Y M Usachev, S A Thayer

Abstract read
In one paragraph

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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Brief low [Mg(2+)]o-induced Ca(2+) spikes inhibit subsequent prolonged exposure-induced excitotoxicity in cultured rat hippocampal neurons.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016
    Article
  5. Article
  6. Article
  7. The upregulation of α2δ-1 subunit modulates activity-dependent Ca2+ signals in sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Y M UsachevDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.
S A Thayer

Funding

NEUROSCIENCE TRAINING IN DRUG ABUSE RESEARCHT32DA007234 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Paul G Mermelstein, Jocelyn M Richard · 1986 to 2026
$10.9M
HIV NEUROTOXICITY--MECHANISM &MODULATION BY CANABINOIDSR01DA007304 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI THAYER, STANLEY A · 1992 to 2024
$5.0M
HIV Neurotoxicity-Mechanism &Modulation by CannabinoidsR37DA007304 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI THAYER, STANLEY A · 2004 to 2013
$3.1M
OPIOID EXCITATORY SIGNALLINGR01DA009293 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI THAYER, STANLEY A · 1996 to 1998
–
NIDA NIH HHS DA07304NIDA NIH HHS DA09293NIDA NIH HHS T32DA07234
6 · The paper itself

Abstract

Ca2+-induced Ca2+ release (CICR) from intracellular stores amplifies the Ca2+ signal that results from depolarization. In neurons, the amplification has been described as a graded process. Here we show that regenerative CICR develops as an all-or-none event in cultured rat dorsal root ganglion neurons in which ryanodine receptors have been sensitized to Ca2+ by caffeine. We used indo-1-based microfluorimetry in combination with whole-cell patch-clamp recording to characterize the relationship between Ca2+ influx and Ca2+ release. Regenerative release of Ca2+ was triggered when action potential-induced Ca2+ influx increased the intracellular Ca2+ concentration ([Ca2+]i) above threshold. The threshold was modulated by caffeine and intraluminal Ca2+. A relative refractory period followed CICR. The pharmacological profile of the response was consistent with Ca2+ influx through voltage-gated Ca2+ channels triggering release from ryanodine-sensitive stores. The activation of a suprathreshold response increased more than fivefold the amplitude and duration of the [Ca2+]i transient. The switch to a suprathreshold response was regulated very precisely in that addition of a single action potential to the stimulus train was sufficient for this transformation. Confocal imaging experiments showed that CICR facilitated propagation of the Ca2+ signal from the plasmalemma to the nucleus. This all-or-none reaction may serve as a switch that determines whether a given electrical signal will be transduced into a local or widespread increase in [Ca2+]i.

Indexed as

Ion Channel GatingAction PotentialsAnimalsCaffeineCalciumCalcium ChannelsCells, CulturedCentral Nervous System StimulantsDifferential ThresholdElectrophysiologyGanglia, SpinalIntracellular MembranesNeurons, AfferentOsmolar ConcentrationRatsRats, Sprague-DawleyCaffeineCalciumCalcium ChannelsCentral Nervous System Stimulants

Identifiers

PMID9295386
PMCPMC6573443

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.