Evidence map›Paper›PMID 24872538›Full record

ArticleJournal of neurophysiology2014

Strychnine-sensitive glycine receptors on pyramidal neurons in layers II/III of the mouse prefrontal cortex are tonically activated.

Michael C Salling, Neil L Harrison

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Ultrafast endocytosis in mouse cortical inhibitory synapses.bioRxiv : the preprint server for biology · 2025
    Article
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  9. Review
  10. Article
  11. Increased Synaptic Strength and mGluAlcoholism, clinical and experimental research · 2021
    Article
  12. Reduced sedation and increased ethanol consumption in knock-in mice expressing an ethanol insensitive alpha 2 subunit of the glycine receptor.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
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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

2 authors at 1 institution in 1 country.

Michael C SallingDepartment of Anesthesiology, Columbia University Medical Center, New York, New York; ms4431@columbia.edu.
Neil L HarrisonDepartment of Anesthesiology, Columbia University Medical Center, New York, New York; Department of Pharmacology, Columbia University, New York, New York.
Columbia University Irving Medical Center · US

Funding

Alcohol and Dopamine Release: Cellular and Synaptic MechanismsR01AA019801 · NIAAA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HARRISON, NEIL L., SULZER, DAVID · 2010 to 2014
$1.8M
Alcohol and inhibition in the prefrontal cortexF32AA022028 · NIAAA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SALLING, MICHAEL CHARLES · 2012 to 2013
$101k
NIAAA NIH HHS F32 AA-022028NIAAA NIH HHS R01 AA-19801
6 · The paper itself

Abstract

Processing of signals within the cerebral cortex requires integration of synaptic inputs and a coordination between excitatory and inhibitory neurotransmission. In addition to the classic form of synaptic inhibition, another important mechanism that can regulate neuronal excitability is tonic inhibition via sustained activation of receptors by ambient levels of inhibitory neurotransmitter, usually GABA. The purpose of this study was to determine whether this occurs in layer II/III pyramidal neurons (PNs) in the prelimbic region of the mouse medial prefrontal cortex (mPFC). We found that these neurons respond to exogenous GABA and to the α4δ-containing GABAA receptor (GABA(A)R)-selective agonist gaboxadol, consistent with the presence of extrasynaptic GABA(A)R populations. Spontaneous and miniature synaptic currents were blocked by the GABA(A)R antagonist gabazine and had fast decay kinetics, consistent with typical synaptic GABA(A)Rs. Very few layer II/III neurons showed a baseline current shift in response to gabazine, but almost all showed a current shift (15-25 pA) in response to picrotoxin. In addition to being a noncompetitive antagonist at GABA(A)Rs, picrotoxin also blocks homomeric glycine receptors (GlyRs). Application of the GlyR antagonist strychnine caused a modest but consistent shift (∼15 pA) in membrane current, without affecting spontaneous synaptic events, consistent with the tonic activation of GlyRs. Further investigation showed that these neurons respond in a concentration-dependent manner to glycine and taurine. Inhibition of glycine transporter 1 (GlyT1) with sarcosine resulted in an inward current and an increase of the strychnine-sensitive current. Our data demonstrate the existence of functional GlyRs in layer II/III of the mPFC and a role for these receptors in tonic inhibition that can have an important influence on mPFC excitability and signal processing.

Indexed as

Neural InhibitionAnimalsGABA AgonistsGlycine AgentsInhibitory Postsynaptic PotentialsMaleMiceMice, Inbred C57BLPrefrontal CortexPyramidal CellsReceptors, GABA-AReceptors, GlycineStrychnineGABA AgonistsGlycine AgentsReceptors, GABA-AReceptors, GlycineStrychnineGABAglycineprefrontal cortextonic current

Identifiers

PMID24872538
PMCPMC4122733
OpenAlexW2034380615

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.