Evidence map›Paper›PMID 21209199›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Glutamate receptor subtypes mediating synaptic activation of prefrontal cortex neurons: relevance for schizophrenia.

Diana C Rotaru, Hiroki Yoshino, David A Lewis, G Bard Ermentrout, Guillermo Gonzalez-Burgos

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 153 citations in OpenAlex.

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  16. mGluNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
    Article
  17. Unsupervised learning for robust working memory.PLoS computational biology · 2022
    Article
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  19. Article
  20. Review

36 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

5 authors at 1 institution in 1 country.

Diana C RotaruTranslational Neuroscience Program, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA.
Hiroki Yoshino
David A Lewis
G Bard Ermentrout
Guillermo Gonzalez-Burgos
University of Pittsburgh · US

Funding

Project 5: In vivo measurement of GABA transmission in healthy controls & subjectP50MH084053 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEWIS, DAVID A · 2008 to 2012
$11.5M
SCHIZOPHRENIA AND CORTICAL DOPAMINE/GABA INTERACTIONSR01MH043784 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEWIS, DAVID A · 1988 to 2023
$7.2M
NIMH NIH HHS MH084053NIMH NIH HHS P50 MH084053NIMH NIH HHS R01 MH043784
6 · The paper itself

Abstract

Schizophrenia may involve hypofunction of NMDA receptor (NMDAR)-mediated signaling, and alterations in parvalbumin-positive fast-spiking (FS) GABA neurons that may cause abnormal gamma oscillations. It was recently hypothesized that prefrontal cortex (PFC) FS neuron activity is highly dependent on NMDAR activation and that, consequently, FS neuron dysfunction in schizophrenia is secondary to NMDAR hypofunction. However, NMDARs are abundant in synapses onto PFC pyramidal neurons; thus, a key question is whether FS neuron or pyramidal cell activation is more dependent on NMDARs. We examined the AMPAR and NMDAR contribution to synaptic activation of FS neurons and pyramidal cells in the PFC of adult mice. In FS neurons, EPSCs had fast decay and weak NMDAR contribution, whereas in pyramidal cells, EPSCs were significantly prolonged by NMDAR-mediated currents. Moreover, the AMPAR/NMDAR EPSC ratio was higher in FS cells. NMDAR antagonists decreased EPSPs and EPSP-spike coupling more strongly in pyramidal cells than in FS neurons, showing that FS neuron activation is less NMDAR dependent than pyramidal cell excitation. The precise EPSP-spike coupling produced by fast-decaying EPSCs in FS cells may be important for network mechanisms of gamma oscillations based on feedback inhibition. To test this possibility, we used simulations in a computational network of reciprocally connected FS neurons and pyramidal cells and found that brief AMPAR-mediated FS neuron activation is crucial to synchronize, via feedback inhibition, pyramidal cells in the gamma frequency band. Our results raise interesting questions about the mechanisms that might link NMDAR hypofunction to alterations of FS neurons in schizophrenia.

Indexed as

Action PotentialsAnimalsBiophysicsComputer SimulationElectric StimulationExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsFemaleGABA AntagonistsIn Vitro TechniquesLysineMaleMembrane PotentialsMiceMice, Inbred C57BLModels, NeurologicalbiocytinExcitatory Amino Acid AntagonistsGABA AntagonistsgabazineLysinePyridazinesReceptors, Glutamate

Identifiers

PMID21209199
PMCPMC3041270
OpenAlexW1988282606

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.