Evidence map›Paper›PMID 22870318›Full record

ArticlePloS one2012

Genetic deletion of NR3A accelerates glutamatergic synapse maturation.

Maile A Henson, Rylan S Larsen, Shelikha N Lawson, Isabel Pérez-Otaño, Nobuki Nakanishi, Stuart A Lipton, Benjamin D Philpot

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

  1. The GluN3-containing NMDA receptors.Channels (Austin, Tex.) · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The roles of GluN3-containing N-methyl-D-aspartate receptor in central nerve system.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Differential impact ofNeurobiology of stress · 2018
    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

7 authors at 3 institutions in 2 countries.

Maile A HensonCurriculum in Neurobiology, University of North Carolina, Chapel Hill, North Carolina, United States of America. maile.henson@nih.gov
Rylan S Larsen
Shelikha N Lawson
Isabel Pérez-Otaño
Nobuki Nakanishi
Stuart A Lipton
Benjamin D Philpot
University of North Carolina at Chapel Hill · USSanford Burnham Prebys Medical Discovery Institute · USUniversidad de Navarra · ES

Funding

PROJECT III - GENETIC APPROACH TO EXCITATORY TRANSMISSIONP01HD029587 · NICHD · SCINTILLON INSTITUTE FOR PHOTOBIOLOGY · PI LIPTON, STUART A · 1992 to 2016
$21.9M
RETINAL GANGLION CELLS: ION CHANNEL &TRANSMITTERSR01EY005477 · NEI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI LIPTON, STUART A · 1985 to 2010
$5.0M
Mechanisms of Presynaptic Plasticity in Visual CortexR01EY018323 · NEI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PHILPOT, BENJAMIN D · 2007 to 2011
$1.8M
NEI NIH HHS R01 EY005477NEI NIH HHS R01 EY018323NEI NIH HHS R01 EY05477NICHD NIH HHS P01 HD029587NICHD NIH HHS P01 HD29687
6 · The paper itself

Abstract

Glutamatergic synapse maturation is critically dependent upon activation of NMDA-type glutamate receptors (NMDARs); however, the contributions of NR3A subunit-containing NMDARs to this process have only begun to be considered. Here we characterized the expression of NR3A in the developing mouse forebrain and examined the consequences of NR3A deletion on excitatory synapse maturation. We found that NR3A is expressed in many subcellular compartments, and during early development, NR3A subunits are particularly concentrated in the postsynaptic density (PSD). NR3A levels dramatically decline with age and are no longer enriched at PSDs in juveniles and adults. Genetic deletion of NR3A accelerates glutamatergic synaptic transmission, as measured by AMPAR-mediated postsynaptic currents recorded in hippocampal CA1. Consistent with the functional observations, we observed that the deletion of NR3A accelerated the expression of the glutamate receptor subunits NR1, NR2A, and GluR1 in the PSD in postnatal day (P) 8 mice. These data support the idea that glutamate receptors concentrate at synapses earlier in NR3A-knockout (NR3A-KO) mice. The precocious maturation of both AMPAR function and glutamate receptor expression are transient in NR3A-KO mice, as AMPAR currents and glutamate receptor protein levels are similar in NR3A-KO and wildtype mice by P16, an age when endogenous NR3A levels are normally declining. Taken together, our data support a model whereby NR3A negatively regulates the developmental stabilization of glutamate receptors involved in excitatory neurotransmission, synaptogenesis, and spine growth.

Indexed as

AgingAnimalsCarrier ProteinsMiceMice, KnockoutNerve Tissue ProteinsPost-Synaptic DensityReceptors, AMPAReceptors, N-Methyl-D-AspartateSpineSynaptic TransmissionCarrier ProteinsGprin1 protein, mouseNerve Tissue ProteinsNR3A NMDA receptorReceptors, AMPAReceptors, N-Methyl-D-Aspartate

Identifiers

PMID22870318
PMCPMC3411625
OpenAlexW2127554180

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.