Evidence map›Paper›PMID 18525022›Full record

ArticleJournal of neurophysiology2008

Prolonged exposure to NMDAR antagonist suppresses inhibitory synaptic transmission in prefrontal cortex.

Yuchun Zhang, M Margarita Behrens, John E Lisman

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

52 citing papers in PubMed, 109 citations in OpenAlex.

  1. Reduced auditory evoked gamma-band response and schizophrenia-like clinical symptoms under subanesthetic ketamine.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
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  11. Integrating Hebbian and homeostatic plasticity: the current state of the field and future research directions.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
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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 at 1 institution in 1 country.

Yuchun ZhangDepartment of Biology and Volen Center for Complex Systems, Brandeis University, MS 008, 415 South Street, Waltham, MA 02454, USA.
M Margarita Behrens
John E Lisman
Brandeis University · US

Funding

NMDA RECEPTOR FUNCTION IN SCHIZOPHRENIAP50MH060450 · NIMH · MC LEAN HOSPITAL (BELMONT, MA) · PI COYLE, JOSEPH T. · 2000 to 2010
$15.4M
NIMH NIH HHS 5P50 MH-060450-08
6 · The paper itself

Abstract

Postmortem studies have shown that schizophrenia produces a reduction in the 67-kilodalton isoform of glutamic acid decarboxylase (GAD67), a key enzyme for gamma-aminobutyric acid (GABA) synthesis. N-methyl-d-aspartate receptor (NMDAR) antagonists have been extensively used to study schizophrenia because they can induce many aspects of the disease, including the decrease in GAD67. It is generally thought that this reduction in GAD implies a reduction in functional inhibition, but direct evidence had been lacking. We have therefore performed physiological studies in slices of prefrontal cortex taken from rats treated with the NMDAR antagonist ketamine. Both frequency and amplitude of miniature inhibitory postsynaptic currents were reduced. Consistent with a reduction of inhibition, we observed an increase in postsynaptic excitability. The increased excitability is likely to result from disinhibition because miniature excitatory postsynaptic current properties and intrinsic excitability were not changed. Ketamine did not affect inhibition or GAD levels in young rats, indicating a developmental regulation that may be related to the developmental increase in ketamine sensitivity that occurs in humans. Our results show that NMDAR antagonist produces biochemical changes in the GABA system that lead to a functional disinhibition. Such disinhibition would be expected to decrease gamma oscillations, which are reduced in schizophrenia.

Indexed as

6-Cyano-7-nitroquinoxaline-2,3-dioneAge FactorsAnimalsDose-Response Relationship, RadiationElectric StimulationExcitatory Amino Acid AntagonistsGene Expression RegulationGlutamate DecarboxylaseInhibitory Postsynaptic PotentialsIn Vitro TechniquesKetamineMaleNeural InhibitionParvalbuminsPrefrontal CortexPyramidal Cells6-Cyano-7-nitroquinoxaline-2,3-dioneExcitatory Amino Acid AntagonistsGlutamate Decarboxylaseglutamate decarboxylase 1KetamineParvalbumins

Identifiers

PMID18525022
PMCPMC2525704
OpenAlexW2161162274

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.