Evidence map›Paper›PMID 19193893›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Coagonist release modulates NMDA receptor subtype contributions at synaptic inputs to retinal ganglion cells.

Trisha L Kalbaugh, Jun Zhang, Jeffrey S Diamond

Abstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
–field-weighted citation impact
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

37 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. NMDARs, Coincidence Detectors of Astrocytic and Neuronal Activities.International journal of molecular sciences · 2021
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Axogenic mechanism enhances retinal ganglion cell excitability during early progression in glaucoma.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  11. Article
  12. Synaptic Mechanisms Generating Orientation Selectivity in the ON Pathway of the Rabbit Retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Organization, control and function of extrasynaptic NMDA receptors.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Review
  18. Article
  19. Article
  20. 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

3 authors.

Trisha L KalbaughSynaptic Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-3701, USA.
Jun Zhang
Jeffrey S Diamond

Funding

Synaptic Mechanisms in the Mammalian RetinaZIANS003039 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI DIAMOND, JEFFREY S · 2009 to 2025
$24.5M
Synaptic Mechanisms in the Mammalian RetinaZ01NS003039 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI DIAMOND, JEFFREY S · 2007 to 2008
$2.8M
Intramural NIH HHS Z01 NS003039
6 · The paper itself

Abstract

NMDA receptors (NMDARs) are tetrameric protein complexes usually comprising two NR1 and two NR2 subunits. Different combinations of four potential NR2 subunits (NR2A-D) confer diversity in developmental expression, subsynaptic localization, and functional characteristics, including affinity for neurotransmitter. NR2B-containing NMDARs, for example, exhibit relatively high affinity both for glutamate and the coagonist glycine. Although multiple NMDAR subtypes can colocalize at individual synapses, particular subtypes often mediate inputs from distinct functional pathways. In retinal ganglion cells (RGCs), NMDARs contribute to synaptic responses elicited by light stimulus onset ("ON") and offset ("OFF"), but roles for particular NMDAR subtypes, and potential segregation between the ON and OFF pathways, have not been explored. Moreover, elements in the retinal circuitry release two different NMDAR coagonists, glycine and d-serine, but the effects of endogenous coagonist release on the relative contribution of different NMDAR subtypes are unclear. Here, we show that coagonist release within the retina modulates the relative contribution of different NMDARs in the ON pathway of the rat retina. By pharmacologically stimulating functional pathways independently in acute slices and recording synaptic responses in RGCs, we show that ON inputs, but not OFF inputs, are mediated in part by NMDARs exhibiting NR2B-like pharmacology. Furthermore, suppressing release of NMDAR coagonist reduces NMDAR activation at ON synapses and increases the relative contribution of these putative NR2B-containing receptors. These results demonstrate direct evidence for evoked coagonist release onto NMDARs and indicate that modulating coagonist release may regulate the relative activation of different NMDAR subtypes in the ON pathway.

Indexed as

AminobutyratesAnimalsExcitatory Amino Acid AgonistsExcitatory Postsynaptic PotentialsMiceMice, TransgenicProtein SubunitsRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateRetinal Ganglion CellsSynapses2-amino-4-phosphonobutyric acidAminobutyratesExcitatory Amino Acid AgonistsProtein SubunitsReceptors, N-Methyl-D-Aspartate

Identifiers

PMID19193893
PMCPMC2650785

What OpenQuestion holds

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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.