Evidence map›Paper›PMID 12879862›Full record

ArticleThe Journal of physiology2003

The plasma membrane calcium-ATPase as a major mechanism for intracellular calcium regulation in neurones from the rat superior cervical ganglion.

N Wanaverbecq, S J Marsh, M Al-Qatari, D A Brown

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-weighted citation impact, top 14% of its field
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

32 citing papers in PubMed, 82 citations in OpenAlex.

  1. Pregabalin acts on NaPain reports · 2026
    Article
  2. Article
  3. Regulation of islet glucagon secretion: Beyond calcium.Diabetes, obesity & metabolism · 2018
    Review
  4. Dynamics of Phosphoinositide-Dependent Signaling in Sympathetic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  5. Trafficking of Na+/Ca2+ exchanger to the site of persistent inflammation in nociceptive afferents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
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  11. Review
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  14. Store-operated Ca2+ entry in sensory neurons: functional role and the effect of painful nerve injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  15. Reactive oxygen species alters the electrophysiological properties and raises [Ca2+]i in intracardiac ganglion neurons.American journal of physiology. Regulatory, integrative and comparative physiology · 2010
    Article
  16. 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

4 authors at 2 institutions in 1 country.

N WanaverbecqDepartment of Pharmacology, University College London, UK. n.wanaverbecq@ion.ucl.ac.uk
S J Marsh
M Al-Qatari
D A Brown
University College London · GBUniversities UK · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Patch-clamp recording combined with indo-l measurement of free intracellular calcium concentration ([Ca2+]i) was used to determine the homeostatic systems involved in the maintenance of resting [Ca2+]I and in the clearance of Ca2+ transients following activation of voltage-gated Ca2+ channels in neurones cultured from rat superior cervical ganglion (SCG). The Ca2+ binding ratio was estimated to be approximately 500 at 100 nM, decreasing to approximately 250 at [Ca2+]i approximately 1 pM, and to involve at least two buffering systems with different affinities for Ca2+. Removal of extracellular Ca2+ led to a decrease in[Ca2+]i that was mimicked by the addition of La3+, and was more pronounced after inhibition of the endoplasmic reticulum Ca2+ uptake system (SERCA). Inhibition of the plasma membrane Ca2+ pump (PMCA) by extracellular allkalinisation (pH 9) or intracellular carboxyeosin both increased resting [Ca2+]i and prolonged the recovery of Ca2+ transients at peak [Ca2+]i C 500 nM. For [Ca2+]i loads >500 nM, recovery showed an additional plateau phase that was abolished i nm-chlorophenylhydrazone (CCCP) or on omitting intracellular Na+. Inhibition of the plasma membrane Na+ -Ca2+ exchanger (NCX) and of SERCA had a small but significant additional effect on the rate of decay of these larger Ca2+ transients. In conclusion, resting [Ca2+]i is maintained by passive Ca2+ influx and regulated by a large Ca2+ buffering system, Ca2+ extrusion via a PMCA and Ca2+ transport from the intracellular stores. PMCA is also the principal Ca2+ extrusion system at low Ca2+ loads, with additional participation of the NCX and intracellular organelles at high [Ca2+]i.

Indexed as

AnimalsBuffersCalciumCalcium-Transporting ATPasesCarrier ProteinsCation Transport ProteinsCells, CulturedElectrophysiologyHomeostasisImmunohistochemistryIntracellular MembranesMitochondriaModels, NeurologicalNeuronsOsmolar ConcentrationPatch-Clamp TechniquesBuffersCalciumCalcium-Transporting ATPasesCarrier ProteinsCation Transport ProteinsPlasma Membrane Calcium-Transporting ATPasesSarcoplasmic Reticulum Calcium-Transporting ATPasesSodium-Calcium Exchangersodium-calcium exchanger 1

Identifiers

PMID12879862
PMCPMC2343008
OpenAlexW2080846302

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.