Evidence map›Paper›PMID 25128575›Full record

ArticleThe Journal of physiology2014

Catecholamine exocytosis during low frequency stimulation in mouse adrenal chromaffin cells is primarily asynchronous and controlled by the novel mechanism of Ca2+ syntilla suppression.

Jason J Lefkowitz, Valerie DeCrescenzo, Kailai Duan, Karl D Bellve, Kevin E Fogarty, John V Walsh, Ronghua ZhuGe

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. How does the stimulus define exocytosis in adrenal chromaffin cells?Pflugers Archiv : European journal of physiology · 2018
    Review
  3. Article
  4. 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

7 authors at 1 institution in 1 country.

Jason J LefkowitzDepartment of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA, 01655, USA.
Valerie DeCrescenzoDepartment of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA, 01655, USA.
Kailai DuanDepartment of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA, 01655, USA.
Karl D BellveBiomedical Imaging Group, University of Massachusetts Medical School, Worcester, MA, 01655, USA Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, 01655, USA.
Kevin E FogartyBiomedical Imaging Group, University of Massachusetts Medical School, Worcester, MA, 01655, USA Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, 01655, USA.
John V WalshDepartment of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA, 01655, USA Biomedical Imaging Group, University of Massachusetts Medical School, Worcester, MA, 01655, USA John.Walsh@umassmed.edu.
Ronghua ZhuGeDepartment of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA, 01655, USA Biomedical Imaging Group, University of Massachusetts Medical School, Worcester, MA, 01655, USA.
University of Massachusetts Chan Medical School · US

Funding

Cellular and Molecular Mechanisms of bitter tastant-induced bronchodilationR01HL117104 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ZHUGE, RONGHUA · 2013 to 2016
$1.6M
Ca2+ Sparks as Regulators of Airway ContractilityR01HL073875 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ZHUGE, RONGHUA · 2004 to 2007
$1.3M
NHLBI NIH HHS HL117104NHLBI NIH HHS HL21697NHLBI NIH HHS HL73875NHLBI NIH HHS R01 HL117104
6 · The paper itself

Abstract

Adrenal chromaffin cells (ACCs), stimulated by the splanchnic nerve, generate action potentials (APs) at a frequency near 0.5 Hz in the resting physiological state, at times described as 'rest and digest'. How such low frequency stimulation in turn elicits sufficient catecholamine exocytosis to set basal sympathetic tone is not readily explained by the classical mechanism of stimulus-secretion coupling, where exocytosis is synchronized to AP-induced Ca(2+) influx. By using simulated action potentials (sAPs) at 0.5 Hz in isolated patch-clamped mouse ACCs, we show here that less than 10% of all catecholaminergic exocytosis, measured by carbon fibre amperometry, is synchronized to an AP. The asynchronous phase, the dominant phase, of exocytosis does not require Ca(2+) influx. Furthermore, increased asynchronous exocytosis is accompanied by an AP-dependent decrease in frequency of Ca(2+) syntillas (i.e. transient, focal Ca(2+) release from internal stores) and is ryanodine sensitive. We propose a mechanism of disinhibition, wherein APs suppress Ca(2+) syntillas, which themselves inhibit exocytosis as they do in the case of spontaneous catecholaminergic exocytosis.

Indexed as

Action PotentialsAdrenal GlandsAnimalsCalciumCalcium SignalingCatecholaminesCells, CulturedChromaffin CellsMaleMicePatch-Clamp TechniquesRyanodine Receptor Calcium Release ChannelCalciumCatecholaminesryanodine receptor 2. mouseRyanodine Receptor Calcium Release Channel

Identifiers

PMID25128575
PMCPMC4253468
OpenAlexW1579639429

What Socratic 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 Socratic graph.