Evidence map›Paper›PMID 27112134›Full record

ArticleThe Journal of physiology2016

GABAB receptors enhance excitatory responses in isolated rat retinal ganglion cells.

Jay Garaycochea, Malcolm M Slaughter

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. The Variety of Mechanosensitive Ion Channels in Retinal Neurons.International journal of molecular sciences · 2024
    Review
  4. Review
  5. CaInternational journal of molecular sciences · 2023
    Review
  6. Mechanisms and Regulation of Neuronal GABACurrent topics in behavioral neurosciences · 2022
    Review
  7. Review
  8. Activation of GABAJournal of neurophysiology · 2020
    Article
  9. Circadian rhythms, refractive development, and myopia.Ophthalmic & physiological optics : the journal of the British College of Ophthalmic Opticians (Optometrists) · 2018
    Review
  10. Article
  11. GABAPhysiological reports · 2017
    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

2 authors at 2 institutions in 1 country.

Jay GaraycocheaNeuroscience Program and Department of Physiology & Biophysics, University at Buffalo School of Medicine, 124 Sherman Hall Buffalo, NY, 14214, USA.
Malcolm M SlaughterNeuroscience Program and Department of Physiology & Biophysics, University at Buffalo School of Medicine, 124 Sherman Hall Buffalo, NY, 14214, USA. mslaught@buffalo.edu.
University at Buffalo, State University of New York · USUniversity of Rochester Medical Center · US

Funding

SYNAPTIC MECHANISMS IN THE VERTEBRATE RETINAR01EY005725 · NEI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SLAUGHTER, MALCOLM M · 1985 to 2012
$4.4M
NEI NIH HHS R01 EY005725
6 · The paper itself

Abstract

key pointsGABA is an inhibitory transmitter but can sometimes produce paradoxical excitatory effects through synaptic networks. We found a novel GABA-mediated excitation within a single retinal cell. It involves a chain of events from receptor stimulation to the sequential modulation of two associated channels, resulting in enhanced neuroexcitability. GABAB receptor activation selectively suppresses N-type calcium channels. The BK-type potassium channels are exclusively linked to the N-type calcium channel. Thus, stimulation of GABAB receptors suppresses an outward current, increasing the excitatory range of single neurons. ABSTRACT: GABAB receptors (GABAB Rs) suppress voltage-gated calcium channels and activate G-protein coupled potassium channels (GIRK and TREK channels), both mechanisms serving to inhibit neurons. In isolated rat retinal spiking neurons, GABAB Rs produce both actions but the net effect is to enhance excitatory signals. This is because GABAB Rs selectively suppress N-type calcium channels, which in turn are specifically linked to BK channels. Consequently, when GABAB Rs are stimulated there is a reduction in outward current, allowing neurons to extend their level of depolarization. Whereas many retinal neurons use L-type channels to stimulate vesicle fusion, the suppression of N-type channels augments dynamic range without affecting transmitter release.

Indexed as

AnimalsCalcium ChannelsFemaleLarge-Conductance Calcium-Activated Potassium ChannelsRats, Sprague-DawleyReceptors, GABA-BRetinal Ganglion CellsCalcium ChannelsLarge-Conductance Calcium-Activated Potassium ChannelsReceptors, GABA-B

Identifiers

PMID27112134
PMCPMC5043044
OpenAlexW2343165166

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.