Evidence map›Paper›PMID 29355693›Full record

ArticleNeuroscience letters2018

Genetic deletion of NMDA receptors suppresses GABAergic synaptic transmission in two distinct types of central neurons.

Xinglong Gu, Wei Lu

Open access · greenAbstract read
In one paragraph

Article in Neuroscience letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Shisa7 phosphorylation regulates GABAergic transmission and neurodevelopmental behaviors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
    Article
  4. Review
  5. Article
  6. Article
  7. Central Actions of 3α,5α-THP Involving NMDA and GABAFrontiers in behavioral neuroscience · 2020
    Article
  8. Review
  9. Genetic Deletion of GABAFrontiers in cellular neuroscience · 2019
    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 1 institution in 1 country.

Xinglong GuSynapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA.
Wei LuSynapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA. Electronic address: luw4@mail.nih.gov.
National Institute of Neurological Disorders and Stroke · US

Funding

The regulation of synaptic transmission and neural circuit functionZIANS003136 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI LU, WEI · 2012 to 2025
$27.0M
Intramural NIH HHS Z99 NS999999Intramural NIH HHS ZIA NS003136
6 · The paper itself

Abstract

NMDA-type ionotropic glutamate receptors (NMDARs) play an important role in the regulation of synapse development and function in the brain. Recently we have shown that NMDARs are critical for GABAergic synapse development in developing hippocampal neurons. However, it remains unclear whether NMDARs are important for establishment of GABAergic synaptic transmission in other types of neurons in the brain. Here we report that in both cortical pyramidal neurons and midbrain dopamine neurons in ventral tegmental area (VTA), genetic deletion of the GluN1 subunit, which is required for assembly of functional NMDARs, leads to a strong reduction of GABAergic synaptic transmission. These data demonstrate that NMDARs play an important role in the development of GABAergic synaptic transmission in two types of neurons with distinct developmental origins, and suggest that NMDARs are commonly involved in development of GABAergic synaptic transmission in different types of neurons in the brain.

Indexed as

AnimalsCerebral CortexDopaminergic Neuronsgamma-Aminobutyric AcidMiceNerve Tissue ProteinsPyramidal CellsReceptors, N-Methyl-D-AspartateSynaptic TransmissionVentral Tegmental Areagamma-Aminobutyric AcidGprin1 protein, mouseNerve Tissue ProteinsReceptors, N-Methyl-D-AspartateCortical pyramidal neuronDopamine neuronGABAergic synapseIn utero electroporationmIPSCNMDA receptorSynapse development

Identifiers

PMID29355693
PMCPMC6136253
OpenAlexW2789772732

What OpenQuestion holds

Textmetadata
LicenceTDM
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.