Evidence map›Paper›PMID 9080362›Full record

ArticleThe Journal of physiology1997

Ca(2+)-induced Ca2+ release mediates Ca2+ transients evoked by single action potentials in rabbit vagal afferent neurones.

A S Cohen, K A Moore, R Bangalore, M S Jafri, D Weinreich, J P Kao

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PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 51 citations in OpenAlex.

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  12. Origin sites of calcium release and calcium oscillations in frog sympathetic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000
    Article
  13. Article
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  15. Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons.Proceedings of the National Academy of Sciences of the United States of America · 1999
    Article
  16. Calcium-induced calcium release contributes to action potential-evoked calcium transients in hippocampal CA1 pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999
    Article
  17. Article
  18. Article
  19. Allergic inflammation in isolated vagal sensory ganglia unmasks silent NK-2 tachykinin receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997
    Article
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

6 authors at 1 institution in 1 country.

A S CohenDepartment of Pharmacology and Experimental Therapeutics, School of Medicine, University of Maryland, Baltimore 21201-1559, USA.
K A Moore
R Bangalore
M S Jafri
D Weinreich
J P Kao
University of Maryland, Baltimore · US

Funding

CHEMORECEPTION AND SIGNAL PROCESSING IN VAGAL AFFERENTSR01NS022069 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI WEINREICH, DANIEL · 1985 to 2006
$1.7M
NOVEL FLUORESCENT PROBES OF CELL SIGNALLING IN MITOSISR29GM046956 · NIGMS · UNIVERSITY OF MARYLAND BALTIMORE · PI KAO, JOSEPH PAO YUNG · 1992 to 1996
–
NIGMS NIH HHS GM 46956NINDS NIH HHS NS 07375NINDS NIH HHS NS 22069
6 · The paper itself

Abstract

1. Standard intracellular recording techniques with 'sharp' micropipettes were used to evoke action potentials (APs) in acutely dissociated adult nodose neurones. 2. APs induced a transient increase in [Ca2+]i (a calcium transient), recorded with fura-2, that was dependent upon [Ca2+]o and the number of APs. Over the range of one to sixty-five APs, the relation between the amplitude of the calcium transient and the number of APs was well fitted by a rectangular hyperbola (chi 2 = 3.53, r = 0.968). From one to four APs, the calcium transient-AP relation can be described by a line with a slope of 9.6 nM AP-1 (r = 0.999). 3. Charge movement corresponding to Ca2+ influx evoked by a single AP was 39 +/- 2.8 pC (mean +/- S.E.M.) and did not change significantly during trains of one to thirty-one APs (P < 0.05). 4. Caffeine (10 mM), a known agonist of the ryanodine receptor, produced an increase in [Ca2+]i. The caffeine-induced rise in [Ca2+]i was attenuated (by > 90%) by lowering [Ca2+]o, and by ryanodine (10 microM), 2,5-di(t-butyl)hydroquinone (DBHQ, 10 microM), or thapsigargin (100 nM). 5. Neurones incubated with ryanodine, DBHQ or thapsigargin required at least eight APs to evoke a detectable calcium transient. These reagents did not significantly affect Ca2+ influx (P < 0.05). In the presence of these inhibitors, the calcium transient-AP relation exhibited slopes of 1.2, 1.1 and 1.9 nM AP-1 for ryanodine, DBHQ and thapsigargin, respectively. When compared with the slope of 9.6 nM AP-1 in non-treated neurones, it appears that Ca2+ influx produced by a single AP is amplified by ca 5- to 10-fold.

Indexed as

Action PotentialsAnimalsCadmiumCaffeineCalciumCalcium-Transporting ATPasesCentral Nervous System StimulantsElectrophysiologyEnzyme InhibitorsFemaleHydroquinonesMaleNeurons, AfferentNodose GanglionRabbitsRyanodine2,5-di-tert-butylhydroquinoneCadmiumCaffeineCalciumCalcium-Transporting ATPasesCentral Nervous System StimulantsEnzyme InhibitorsHydroquinonesRyanodineThapsigargin

Identifiers

PMID9080362
PMCPMC1159307
OpenAlexW2140207877

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.