Evidence map›Paper›PMID 27254001›Full record

ArticleEndocrinology2016

Glucocorticoids Inhibit CRH/AVP-Evoked Bursting Activity of Male Murine Anterior Pituitary Corticotrophs.

Peter J Duncan, Joël Tabak, Peter Ruth, Richard Bertram, Michael J Shipston

Open access · hybridAbstract read
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  5. Fast dynamics in the HPA axis: Insight from mathematical and experimental studies.Current opinion in endocrine and metabolic research · 2022
    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

5 authors at 4 institutions in 3 countries.

Peter J DuncanCentre for Integrative Physiology (P.J.D., M.J.S.), College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh EH8 9XD, United Kingdom; Biomedical Neuroscience Research Group (J.T.), University of Exeter Medical School, Exeter EX4 4PL, United Kingdom; Division of Pharmacology, Toxicology, and Clinical Pharmacy (P.R.), Institute for Pharmacy, University of Tübingen, D-72076 Tübingen, Germany; and Department of Mathematics and Programs in Neuroscience and Molecular Biophysics (R.B.), Florida State University, Tallahassee, Florida 32306.
Joël TabakCentre for Integrative Physiology (P.J.D., M.J.S.), College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh EH8 9XD, United Kingdom; Biomedical Neuroscience Research Group (J.T.), University of Exeter Medical School, Exeter EX4 4PL, United Kingdom; Division of Pharmacology, Toxicology, and Clinical Pharmacy (P.R.), Institute for Pharmacy, University of Tübingen, D-72076 Tübingen, Germany; and Department of Mathematics and Programs in Neuroscience and Molecular Biophysics (R.B.), Florida State University, Tallahassee, Florida 32306.
Peter RuthCentre for Integrative Physiology (P.J.D., M.J.S.), College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh EH8 9XD, United Kingdom; Biomedical Neuroscience Research Group (J.T.), University of Exeter Medical School, Exeter EX4 4PL, United Kingdom; Division of Pharmacology, Toxicology, and Clinical Pharmacy (P.R.), Institute for Pharmacy, University of Tübingen, D-72076 Tübingen, Germany; and Department of Mathematics and Programs in Neuroscience and Molecular Biophysics (R.B.), Florida State University, Tallahassee, Florida 32306.
Richard BertramCentre for Integrative Physiology (P.J.D., M.J.S.), College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh EH8 9XD, United Kingdom; Biomedical Neuroscience Research Group (J.T.), University of Exeter Medical School, Exeter EX4 4PL, United Kingdom; Division of Pharmacology, Toxicology, and Clinical Pharmacy (P.R.), Institute for Pharmacy, University of Tübingen, D-72076 Tübingen, Germany; and Department of Mathematics and Programs in Neuroscience and Molecular Biophysics (R.B.), Florida State University, Tallahassee, Florida 32306.
Michael J ShipstonCentre for Integrative Physiology (P.J.D., M.J.S.), College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh EH8 9XD, United Kingdom; Biomedical Neuroscience Research Group (J.T.), University of Exeter Medical School, Exeter EX4 4PL, United Kingdom; Division of Pharmacology, Toxicology, and Clinical Pharmacy (P.R.), Institute for Pharmacy, University of Tübingen, D-72076 Tübingen, Germany; and Department of Mathematics and Programs in Neuroscience and Molecular Biophysics (R.B.), Florida State University, Tallahassee, Florida 32306.
University of Edinburgh · GBFlorida State University · USUniversity of Exeter · GBUniversity of Tübingen · DE

Funding

REGULATION OF PROLACTIN SECRETION AT THE LACTOTROPHR01DK043200 · NIDDK · FLORIDA STATE UNIVERSITY · PI BERTRAM, RICHARD, GONZALEZ-IGLESIAS, ARTURO EDUARDO · 1992 to 2014
$4.9M
NIDDK NIH HHS R01 DK043200Wellcome Trust
6 · The paper itself

Abstract

Corticotroph cells from the anterior pituitary are an integral component of the hypothalamic-pituitary-adrenal (HPA) axis, which governs the neuroendocrine response to stress. Corticotrophs are electrically excitable and fire spontaneous single-spike action potentials and also display secretagogue-induced bursting behavior. The HPA axis function is dependent on effective negative feedback in which elevated plasma glucocorticoids result in inhibition at the level of both the pituitary and the hypothalamus. In this study, we have used an electrophysiological approach coupled with mathematical modeling to investigate the regulation of spontaneous and CRH/arginine vasopressin-induced activity of corticotrophs by glucocorticoids. We reveal that pretreatment of corticotrophs with 100 nM corticosterone (CORT; 90 and 150 min) reduces spontaneous activity and prevents a transition from spiking to bursting after CRH/arginine vasopressin stimulation. In addition, previous studies have identified a role for large-conductance calcium- and voltage-activated potassium (BK) channels in the generation of secretagogue-induced bursting in corticotrophs. Using the dynamic clamp technique, we demonstrated that CRH-induced bursting can be switched to spiking by subtracting a fast BK current, whereas the addition of a fast BK current can induce bursting in CORT-treated cells. In addition, recordings from BK knockout mice (BK(-/-)) revealed that CORT can also inhibit excitability through BK-independent mechanisms to control spike frequency. Thus, we have established that glucocorticoids can modulate multiple properties of corticotroph electrical excitability through both BK-dependent and BK-independent mechanisms.

Indexed as

AnimalsArginine VasopressinCells, CulturedCorticotrophsCorticotropin-Releasing HormoneDown-RegulationEvoked PotentialsGlucocorticoidsLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMaleMiceMice, Inbred C57BLMice, KnockoutPituitary Gland, AnteriorArginine VasopressinCorticotropin-Releasing HormoneGlucocorticoidsLarge-Conductance Calcium-Activated Potassium Channel alpha Subunits

Identifiers

PMID27254001
PMCPMC4967125
OpenAlexW2410660255

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.