Evidence map›Paper›PMID 30901926›Full record

ReviewInternational journal of molecular sciences2019

NMDA Receptor Model of Antipsychotic Drug-Induced Hypofrontality.

Marek Krzystanek, Artur Pałasz

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
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  5. Pharmacological reduction of reverse-translated hippocampal hyperactivity in mouse: relevance for psychosis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  6. Article
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  9. Genetic mechanisms for impaired synaptic plasticity in schizophrenia revealed by computational modeling.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Discovery of GluN2A subtype-selectiveActa pharmaceutica Sinica. B · 2024
    Review
  11. Article
  12. Article
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  14. Review
  15. Article
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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

2 authors.

Marek KrzystanekDepartment and Clinic of Psychiatric Rehabilitation, Department of Psychiatry and Psychotherapy, School of Medicine in Katowice, Ziołowa 45/47, 40-635 Katowice, Poland. krzystanekmarek@gmail.com.ORCID 0000-0002-1665-7344
Artur PałaszDepartment of Histology, School of Medicine in Katowice, Medyków 18, 40-752 Katowice, Poland. artiassone@gmail.com.

Funding

Polish National Centre for Research and Development POIG.01.04.00-04-219/12
6 · The paper itself

Abstract

Schizophrenia is a chronic mental disease, affecting around 1% of the general population. Schizophrenia is characterized by productive, negative, affective, and disorganization symptoms, and cognitive deficits. Cognitive deficits prevail in most of the schizophrenia patients and are one of the most disabling symptoms. They usually occur before the acute episode of the disease and tend to become chronic with no satisfactory treatment from antipsychotic drugs. Because of their early manifestation in patients' lives, cognitive deficits are suggested to be the primary symptom of schizophrenia. The pathogenesis of cognitive deficits in schizophrenia is not fully understood. They are linked with hypofrontality, which is a decrease in blood flow and glucose metabolism in the prefrontal lobe of schizophrenia-suffering patients. Hypofrontality is linked with disturbances of the corticolimbothalamic circuit, important for cognition and memory in humans. The circuit consists of a group of neuroanatomic structures and hypothetically any disturbance in them may result in cognitive deficits. We present a translational preclinical model of understanding how antipsychotic medication may decrease the N-methyl-D-aspartic acid (NMDA) receptors' activity and produce dysfunctions in the corticolimbothalamic circuit and hypofrontality. From several pharmacological experiments on rats, including mainly our own recent findings, we collected data that suggest that antipsychotic medication may maintain and escalate hypofrontality in schizophrenia, decreasing NMDA receptor activity in the corticolimbothalamic circuit in the human brain. We discuss our findings within the literature of the subject.

Indexed as

AnimalsAntipsychotic AgentsCognitionCognition DisordersGene Expression RegulationGlutamatesHumansPrefrontal CortexReceptors, N-Methyl-D-AspartateSchizophreniaSignal TransductionSynaptic TransmissionAntipsychotic AgentsGlutamatesReceptors, N-Methyl-D-Aspartateantipsychotic drugshypofrontalityNMDA receptorschizophrenia

Identifiers

PMID30901926
PMCPMC6471005
OpenAlexW2924261055

What OpenQuestion holds

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LicenceCC BY
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.