Evidence map›Paper›PMID 22009744›Full record

ArticleThe Journal of biological chemistry2011

Pituitary adenylate cyclase-activating peptide (PACAP) recruits low voltage-activated T-type calcium influx under acute sympathetic stimulation in mouse adrenal chromaffin cells.

Jacqueline Hill, Shyue-An Chan, Barbara Kuri, Corey Smith

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 19% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

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  15. PACAP signaling in stress: insights from the chromaffin cell.Pflugers Archiv : European journal of physiology · 2018
    Review
  16. L-type calcium channels in exocytosis and endocytosis of chromaffin cells.Pflugers Archiv : European journal of physiology · 2018
    Review
  17. Roles of NaPflugers Archiv : European journal of physiology · 2018
    Review
  18. Review
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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 1 institution in 1 country.

Jacqueline HillDepartment of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106.
Shyue-An ChanDepartment of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106.
Barbara KuriDepartment of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106.
Corey SmithDepartment of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106. Electronic address: Corey.Smith@Case.Edu.
Case Western Reserve University · US

Funding

HEART-LUNG PHYSIOLOGY: MOLECULAR-SYSTEMIC INTEGRATIONT32HL007887 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI SCHILLING, WILLIAM P · 1999 to 2008
$2.5M
NHLBI NIH HHS T32 HL007887NHLBI NIH HHS T32 HL 07887
6 · The paper itself

Abstract

Low voltage-activated T-type Ca(v)3.2 calcium channels are expressed in neurosecretory chromaffin cells of the adrenal medulla. Previous studies have shown that naïve adrenal chromaffin cells express a nominal Ca(v)3.2-dependent conductance. However, Ca(v)3.2 conductance is up-regulated following chronic hypoxia or long term exposure to cAMP analogs. Thus, although a link between chronic stressors and up-regulation of Ca(v)3.2 exists, there are no reports testing the specific role of Ca(v)3.2 channels in the acute sympathoadrenal stress response. In this study, we examined the effects of acute sympathetic stress on T-type Ca(v)3.2 calcium influx in mouse chromaffin cells in situ. Pituitary adenylate cyclase-activating peptide (PACAP) is an excitatory neuroactive peptide transmitter released by the splanchnic nerve under elevated sympathetic activity to stimulate the adrenal medulla. PACAP stimulation did not evoke action potential firing in chromaffin cells but did cause a persistent subthreshold membrane depolarization that resulted in an immediate and robust Ca(2+)-dependent catecholamine secretion. Moreover, PACAP-evoked secretion was sensitive to block by nickel chloride and was acutely inhibited by protein kinase C blockers. We utilized perforated patch electrophysiological recordings conducted in adrenal tissue slices to investigate the mechanism of PACAP-evoked calcium entry. We provide evidence that stimulation with exogenous PACAP and native neuronal stress stimulation both lead to a protein kinase C-mediated phosphodependent recruitment of a T-type Ca(v)3.2 Ca(2+) influx. This in turn evokes catecholamine release during the acute sympathetic stress response.

Indexed as

Adrenal MedullaAnimalsCalciumCalcium Channels, T-TypeCatecholaminesChromaffin CellsElectrophysiologyImmunohistochemistryMaleMiceMice, Inbred C57BLNeuronsNickelPituitary Adenylate Cyclase-Activating PolypeptideProtein Kinase CSympathetic Nervous SystemCacna1h protein, mouseCalciumCalcium Channels, T-TypeCatecholaminesNickelPituitary Adenylate Cyclase-Activating PolypeptideProtein Kinase C

Identifiers

PMID22009744
PMCPMC3234986
OpenAlexW2024958741

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.