Evidence map›Paper›PMID 27147972›Full record

ReviewFrontiers in cellular neuroscience2016

GABA Signaling and Neuroactive Steroids in Adrenal Medullary Chromaffin Cells.

Keita Harada, Hidetada Matsuoka, Hiroaki Fujihara, Yoichi Ueta, Yuchio Yanagawa, Masumi Inoue

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Genome-wide screening for genetic variants in polyadenylation signal (PAS) sites in mouse selection lines for fatness and leanness.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. GABAPflugers Archiv : European journal of physiology · 2018
    Review
  12. Article
  13. Article
  14. 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 2 institutions in 1 country.

Keita HaradaDepartment of Cell and Systems Physiology, University of Occupational and Environmental Health School of Medicine Kitakyushu, Japan.
Hidetada MatsuokaDepartment of Cell and Systems Physiology, University of Occupational and Environmental Health School of Medicine Kitakyushu, Japan.
Hiroaki FujiharaDepartment of Physiology, University of Occupational and Environmental Health School of Medicine Kitakyushu, Japan.
Yoichi UetaDepartment of Physiology, University of Occupational and Environmental Health School of Medicine Kitakyushu, Japan.
Yuchio YanagawaDepartment of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine Maebashi, Japan.
Masumi InoueDepartment of Cell and Systems Physiology, University of Occupational and Environmental Health School of Medicine Kitakyushu, Japan.
University of Occupational and Environmental Health Japan · JPGunma University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gamma-aminobutyric acid (GABA) is produced not only in the brain, but also in endocrine cells by the two isoforms of glutamic acid decarboxylase (GAD), GAD65 and GAD67. In rat adrenal medullary chromaffin cells only GAD67 is expressed, and GABA is stored in large dense core vesicles (LDCVs), but not synaptic-like microvesicles (SLMVs). The α3β2/3γ2 complex represents the majority of GABAA receptors expressed in rat and guinea pig chromaffin cells, whereas PC12 cells, an immortalized rat chromaffin cell line, express the α1 subunit as well as the α3. The expression of α3, but not α1, in PC12 cells is enhanced by glucocorticoid activity, which may be mediated by both the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR). GABA has two actions mediated by GABAA receptors in chromaffin cells: it induces catecholamine secretion by itself and produces an inhibition of synaptically evoked secretion by a shunt effect. Allopregnanolone, a neuroactive steroid which is secreted from the adrenal cortex, produces a marked facilitation of GABAA receptor channel activity. Since there are no GABAergic nerve fibers in the adrenal medulla, GABA may function as a para/autocrine factor in the chromaffin cells. This function of GABA may be facilitated by expression of the immature isoforms of GAD and GABAA receptors and the lack of expression of plasma membrane GABA transporters (GATs). In this review, we will consider how the para/autocrine function of GABA is achieved, focusing on the structural and molecular mechanisms for GABA signaling.

Indexed as

adrenal chromaffin cellGABAGABAA receptorsGAD67immature subunitneuroactive steroidparacrinePC12 cell

Identifiers

PMID27147972
PMCPMC4834308
OpenAlexW2336643662

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.