Evidence map›Paper›PMID 28592413›Full record

ArticleAmerican journal of physiology. Cell physiology2017

Recruitment of endosomal signaling mediates the forskolin modulation of guinea pig cardiac neuron excitability.

Jean C Hardwick, Todd A Clason, John D Tompkins, Beatrice M Girard, Caitlin N Baran, Laura A Merriam, Victor May, Rodney L Parsons

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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

8 authors at 3 institutions in 1 country.

Jean C HardwickDepartment of Biology, Ithaca College, Ithaca, New York.
Todd A ClasonDepartment of Neurological Sciences, Robert Larner MD College of Medicine, University of Vermont, Burlington, Vermont.
John D TompkinsDepartment of Medicine (Cardiology), David Geffen School of Medicine, University of California, Los Angeles, California; and.
Beatrice M GirardDepartment of Neurological Sciences, Robert Larner MD College of Medicine, University of Vermont, Burlington, Vermont.
Caitlin N BaranDepartment of Medicine, Robert Larner MD College of Medicine, University of Vermont, Burlington, Vermont.
Laura A MerriamDepartment of Neurological Sciences, Robert Larner MD College of Medicine, University of Vermont, Burlington, Vermont.
Victor MayDepartment of Neurological Sciences, Robert Larner MD College of Medicine, University of Vermont, Burlington, Vermont.
Rodney L ParsonsDepartment of Neurological Sciences, Robert Larner MD College of Medicine, University of Vermont, Burlington, Vermont; Rodney.Parsons@med.uvm.edu.
University of Vermont · USIthaca College · USUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Forskolin, a selective activator of adenylyl cyclase (AC), commonly is used to establish actions of G protein-coupled receptors (GPCRs) that are initiated primarily through activation of AC/cAMP signaling pathways. In the present study, forskolin was used to evaluate the potential role of AC/cAMP, which is a major signaling mechanism for the pituitary adenylate cyclase-activating polypeptide (PACAP)-selective PAC1 receptor, in the regulation of guinea pig cardiac neuronal excitability. Forskolin (5-10 µM) increases excitability in ~60% of the cardiac neurons. The forskolin-mediated increase in excitability was considered related to cAMP regulation of a cyclic nucleotide gated channel or via protein kinase A (PKA)/ERK signaling, mechanisms that have been linked to PAC1 receptor activation. However, unlike PACAP mechanisms, forskolin enhancement of excitability was not significantly reduced by treatment with cesium to block currents through hyperpolarization-activated nonselective cation channels (

Indexed as

Adenylyl CyclasesAnimalsCarbazolesClathrinColforsinCyclic AMPCyclic AMP-Dependent Protein KinasesEndosomesFlavonoidsGuinea PigsHeartHumansMAP Kinase Signaling SystemMyocardiumNeuronsPituitary Adenylate Cyclase-Activating Polypeptide2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneAdenylyl CyclasesCarbazolesClathrinColforsinCyclic AMPCyclic AMP-Dependent Protein KinasesFlavonoidsKT 5720Pituitary Adenylate Cyclase-Activating PolypeptidePyrrolesReceptors, G-Protein-CoupledReceptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type Iautonomic neuronforskolinMAPK signalingneuronal excitabilityPKA

Identifiers

PMID28592413
PMCPMC5582876
OpenAlexW2622920666

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.