Evidence map›Paper›PMID 10460241›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Junctional versus extrajunctional glycine and GABA(A) receptor-mediated IPSCs in identified lamina I neurons of the adult rat spinal cord.

N Chéry, Y de Koninck

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

75 citing papers in PubMed, 203 citations in OpenAlex.

  1. Review
  2. Competition between glycine and GABAProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. GABACells · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. PKCγ interneurons, a gateway to pathological pain in the dorsal horn.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Review
  13. Reviewing the case for compromised spinal inhibition in neuropathic pain.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Corelease of Inhibitory Neurotransmitters in the Mouse Auditory Midbrain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  19. Review
  20. Article

15 more citing papers are in PubMed but not listed here.

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.

N ChéryDepartment of Pharmacology and Therapeutics, McGill University, Montréal, Québec, H3G 1Y6 Canada.
Y de Koninck
McGill University · CA

Funding

INHIBITORY MECHANISMS IN THE SPINAL DORSAL HORNR01NS034022 · NINDS · MCGILL UNIVERSITY · PI DE KONINCK, YVES · 1996 to 1998
–
NINDS NIH HHS NS 34022
6 · The paper itself

Abstract

Colocalization of GABA and glycine in synaptic terminals of the superficial dorsal horn raises the question of their relative contribution to inhibition of different classes of neurons in this area. To address this issue, miniature IPSCs (mIPSCs) mediated via GABA(A) receptors (GABA(A)Rs) and glycine receptors (GlyRs) were recorded from identified laminae I-II neurons in adult rat spinal cord slices. GABA(A)R-mediated mIPSCs had similar amplitude and rise times, but significantly slower decay kinetics than GlyR-mediated mIPSCs. Lamina I neurons appeared to receive almost exclusively GlyR-mediated mIPSCs, even after application of hypertonic solutions. Yet, all neurons responded to exogenous applications of both GABA and glycine, indicating that they expressed both GABA(A)Rs and GlyRs. Given that virtually all glycinergic interneurons also contain GABA, the possibility was examined that GABA(A)Rs may be located extrasynaptically in lamina I neurons. A slow GABA(A)R-mediated component was revealed in large, but not minimally evoked monosynaptic IPSCs. Administration of the benzodiazepine flunitrazepam unmasked a GABA(A)R component to most mIPSCs, suggesting that both transmitters were released from the same vesicle. The isolated GABA(A)R component of these mIPSCs had rising kinetics 10 times slower than that of the GlyR component (or of GABA(A)R mIPSCs in lamina II). The slow GABA(A)R components were prolonged by GABA uptake blockers. It is concluded that, whereas GABA and glycine are likely released from the same vesicle of transmitter in lamina I, GABA(A)Rs appear to be located extrasynaptically. Thus, glycine mediates most of the tonic inhibition at these synapses. This differential distribution of GABA(A)Rs and GlyRs confers distinct functional properties to inhibition mediated by these two transmitters in lamina I.

Indexed as

2-Amino-5-phosphonovalerate6-Cyano-7-nitroquinoxaline-2,3-dioneAnimalsBicucullineEvoked PotentialsFlunitrazepamGABA Antagonistsgamma-Aminobutyric AcidGlycineIn Vitro TechniquesMaleNeuronsPatch-Clamp TechniquesPyridazinesRatsRats, Sprague-Dawley2-Amino-5-phosphonovalerate6-Cyano-7-nitroquinoxaline-2,3-dioneBicucullineFlunitrazepamGABA Antagonistsgabazinegamma-Aminobutyric AcidGlycinePyridazinesReceptors, GABA-AReceptors, GlycineStrychnineSucroseTetrodotoxin

Identifiers

PMID10460241
PMCPMC6782499
OpenAlexW1866618643

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.