Evidence map›Paper›PMID 10234003›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

A current activated on depletion of intracellular Ca2+ stores can regulate exocytosis in adrenal chromaffin cells.

A F Fomina, M C Nowycky

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Review
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  4. CRAC channelopathies.Pflugers Archiv : European journal of physiology · 2010
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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.

A F FominaDepartment of Neurobiology and Anatomy, Medical College of Pennsylvania Hahnemann University, Philadelphia, Pennsylvania 19129, USA.
M C Nowycky

Funding

MODULATION AND REGULATION OF NEURONAL CALCIUM CHANNELSR01NS022281 · NINDS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI NOWYCKY, MARTHA C · 1985 to 1998
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NINDS NIH HHS NS22281
6 · The paper itself

Abstract

Exocytosis in excitable cells is strongly coupled to Ca2+ entry through voltage-gated channels but can be evoked by activation of membrane receptors that release Ca2+ from inositol 1,4, 5-trisphosphate-sensitive internal stores. In many cell types, depletion of Ca2+ stores activates Ca2+ influx across the plasma membrane, a process known as capacitative or store-operated Ca2+ entry. This influx is mediated by a number of voltage-independent, Ca2+-selective currents. In addition to replenishing Ca2+ stores, these currents are hypothesized to play an important role in agonist-evoked secretion in nonexcitable cells, although this has not been confirmed experimentally. The existence and physiological function of such currents in excitable cells is not known. Using the capacitance detection technique to monitor exocytosis, we provide direct experimental evidence that a similar mechanism exists in bovine adrenal chromaffin cells. Depletion of intracellular Ca2+ stores with thapsigargin, a SERCA pump inhibitor, or with BAPTA, an exogenous Ca2+ chelator, activates a small-amplitude, voltage-independent current that is carried by Ca2+ and Na+ ions. Ca2+ entry through this pathway is sufficient to stimulate exocytosis at negative membrane potentials. In addition, depolarization-evoked exocytosis is markedly facilitated on activation of the current. These data suggest that excitable cells possess a store-operated Ca2+ influx mechanism that may both directly trigger exocytosis and modulate excitation-secretion coupling.

Indexed as

AnimalsCalciumCatecholaminesCattleChelating AgentsChromaffin CellsEgtazic AcidElectric ConductivityExocytosisLiposomesMembrane PotentialsPatch-Clamp TechniquesThapsigargin1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidCalciumCatecholaminesChelating AgentsEgtazic AcidLiposomesThapsigargin

Identifiers

PMID10234003
PMCPMC6782721

What OpenQuestion holds

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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.