Evidence map›Paper›PMID 20880830›Full record

ReviewClinical schizophrenia & related psychoses2010

Thinking glutamatergically: changing concepts of schizophrenia based upon changing neurochemical models.

Joshua T Kantrowitz, Daniel C Javitt

Open access · greenAbstract readReview
In one paragraph

Review in Clinical schizophrenia & related psychoses, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 118 citations in OpenAlex.

  1. Trial
  2. Mismatch negativity encoding of prediction errors predicts S-ketamine-induced cognitive impairments.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012
    Trial
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Targeting Serotonin 5-HTCNS drugs · 2020
    Review
  9. Article
  10. NMDA Receptor Model of Antipsychotic Drug-Induced Hypofrontality.International journal of molecular sciences · 2019
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Diverse Effects on MACS chemical neuroscience · 2017
    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

2 authors at 2 institutions in 1 country.

Joshua T KantrowitzSchizophrenia Research Center, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA.
Daniel C Javitt
Nathan Kline Institute for Psychiatric Research · USNew York University · US

Funding

EARLY CORTICAL PROCESSING IN SCHIZOPHRENIAR01MH049334 · NIMH · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI JAVITT, DANIEL C. · 1998 to 2022
$8.8M
Early Cortical Processing In SchizophreniaR37MH049334 · NIMH · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI JAVITT, DANIEL C. · 2003 to 2012
$4.2M
PHENCYCLIDINE ABUSE &PSYCHOSIS--BIOMEDICAL MECHANISMSR01DA003383 · NIDA · YESHIVA UNIVERSITY · PI JAVITT, DANIEL C. · 1985 to 2010
$3.2M
NIDA NIH HHS R01 DA003383NIDA NIH HHS R01DA03383NIMH NIH HHS L30 MH084666NIMH NIH HHS R01 MH049334NIMH NIH HHS R37 MH049334NIMH NIH HHS R37 MH49334
6 · The paper itself

Abstract

Clinical concepts of mental illness have always been modulated by underlying theoretical considerations. For the past fifty years, schizophrenia has been considered primarily a disease of dopaminergic neurotransmission. Although this conceptualization has helped greatly in explaining the clinical effects of psychostimulants and guiding the clinical use of both typical and atypical antipsychotics, it has nevertheless shaded how we look at the disorder from both a pathophysiological and therapeutic perspective. For example, most explanatory research in schizophrenia has focused on dopamine-rich regions of the brain, with little investigation of regions of the brain that are relatively dopamine poor. Starting approximately twenty years ago, an alternative formulation of schizophrenia was proposed based upon actions of the "dissociative anesthetic" class of psychotomimetic agents, including phencyclidine (PCP), ketamine and various designer drugs. These compounds induce psychosis by blocking neurotransmission at N-methyl-D-aspartate (NMDA)-type glutamate receptors, suggesting an alternative model for pathogenesis in schizophrenia. As opposed to dopamine, the glutamatergic system is widely distributed throughout the brain and plays a prominent role in sensory processing as well as in subsequent stages of cortical analysis. Glutamatergic theories of schizophrenia, thus, predict that cortical dysfunction will be regionally diffuse but process specific. In addition, NMDA receptors incorporate binding sites for specific endogenous brain compounds, including the amino acids glycine and D-serine and the redox modulator glutathione, and interact closely with dopaminergic, cholinergic and γ-aminobutyric acid (GABA)-ergic systems. Glutamatergic theories, thus, open new potential approaches for treatment of schizophrenia, most of which are only now entering clinical evaluation.

Indexed as

Models, NeurologicalBrainGlutamic AcidHumansModels, ChemicalReceptors, N-Methyl-D-AspartateSchizophreniaGlutamic AcidReceptors, N-Methyl-D-Aspartate

Identifiers

PMID20880830
PMCPMC4988235
OpenAlexW2054802990

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.