Evidence map›Paper›PMID 20107067›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Serine racemase deletion protects against cerebral ischemia and excitotoxicity.

Asif K Mustafa, Abdullah S Ahmad, Emil Zeynalov, Sadia K Gazi, Gautam Sikka, Jeffrey T Ehmsen, Roxanne K Barrow, Joseph T Coyle, Solomon H Snyder, Sylvain Doré

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
–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

45 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Review
  4. Review
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  8. Review
  9. Information-Rich, Dual-FunctionJournal of the American Chemical Society · 2023
    Article
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  11. Article
  12. Review
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  18. The Role of Serine Racemase in the Pathophysiology of Brain Disorders.Advances in pharmacology (San Diego, Calif.) · 2018
    Review
  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

10 authors.

Asif K MustafaSolomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Abdullah S Ahmad
Emil Zeynalov
Sadia K Gazi
Gautam Sikka
Jeffrey T Ehmsen
Roxanne K Barrow
Joseph T Coyle
Solomon H Snyder
Sylvain Doré

Funding

NMDA RECEPTOR FUNCTION IN SCHIZOPHRENIAP50MH060450 · NIMH · MC LEAN HOSPITAL (BELMONT, MA) · PI COYLE, JOSEPH T. · 2000 to 2010
$15.4M
NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGSR37MH018501 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1990 to 2009
$11.5M
NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGSR01MH018501 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1985 to 2019
$10.8M
PSYCHOSIS AND BRAIN GLUTAMATER01MH051290 · NIMH · MC LEAN HOSPITAL (BELMONT, MA) · PI COYLE, JOSEPH T. · 1994 to 2017
$5.0M
PG receptors in controling excitotoxicity in aging brainR01AG022971 · NIA · JOHNS HOPKINS UNIVERSITY · PI DORE, SYLVAIN · 2004 to 2008
$1.6M
NEUROTRANSMITTER RECEPTORSK05DA000074 · NIDA · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1985 to 2009
$1.3M
Regulation of D-serine Neuromodulation by PKCalpha and PICK1F30MH074191 · NIMH · JOHNS HOPKINS UNIVERSITY · PI MUSTAFA, ASIF K · 2006 to 2009
$156k
NIA NIH HHS AG022971NIA NIH HHS R01 AG022971NIDA NIH HHS K05 DA000074NIMH NIH HHS 1 F30 MH074191-01A2NIMH NIH HHS F30 MH074191NIMH NIH HHS MH18501NIMH NIH HHS MH-572901NIMH NIH HHS P50 MH060450NIMH NIH HHS R01 MH018501NIMH NIH HHS R01 MH051290NIMH NIH HHS R37 MH018501
6 · The paper itself

Abstract

D-Serine, formed from L-serine by serine racemase (SR), is a physiologic coagonist at NMDA receptors. Using mice with targeted deletion of SR, we demonstrate a role for D-serine in NMDA receptor-mediated neurotoxicity and stroke. Brain cultures of SR-deleted mice display markedly diminished nitric oxide (NO) formation and neurotoxicity. In intact SR knock-out mice, NO formation and nitrosylation of NO targets are substantially reduced. Infarct volume following middle cerebral artery occlusion is dramatically diminished in several regions of the brains of SR mutant mice despite evidence of increased NMDA receptor number and sensitivity.

Indexed as

AnimalsBrainBrain InfarctionBrain IschemiaCells, CulturedCytoprotectionDisease Models, AnimalDown-RegulationGene DeletionGene Expression Regulation, EnzymologicGenetic TherapyInfarction, Middle Cerebral ArteryIsomerismMaleMiceMice, KnockoutNeurotoxinsNitric OxideNitric Oxide Synthase Type INitro CompoundsRacemases and EpimerasesReceptors, N-Methyl-D-AspartateSerineSerine Racemase

Identifiers

PMID20107067
PMCPMC2841469

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.