Evidence map›Paper›PMID 29936230›Full record

ReviewNeurobiology of disease2019

Alterations in cortical interneurons and cognitive function in schizophrenia.

Samuel J Dienel, David A Lewis

Abstract readReview
In one paragraph

Review in Neurobiology of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed
–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

176 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Aperiodic Signatures of Stress Sensitivity and Depression Recurrence in Adolescents.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2026
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

116 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

2 authors.

Samuel J DienelMedical Scientist Training Program, University of Pittsburgh, United States; Translational Neuroscience Program, Department of Psychiatry, School of Medicine, University of Pittsburgh, United States.
David A LewisTranslational Neuroscience Program, Department of Psychiatry, School of Medicine, University of Pittsburgh, United States; Department of Neuroscience, Dietrich School of Arts and Sciences, University of Pittsburgh, United States. Electronic address: lewisda@upmc.edu.

Funding

TRAINING PROGRAM FOR MD/PHD STUDENTST32GM008208 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STEINMAN, RICHARD A · 1987 to 2021
$15.4M
Statistics and Data Management CoreP50MH103204 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OLSON, CARL ROGER · 2014 to 2018
$10.8M
SCHIZOPHRENIA AND CORTICAL DOPAMINE/GABA INTERACTIONSR01MH043784 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEWIS, DAVID A · 1988 to 2023
$7.2M
GABA Neurons and Cortical Circuitry in SchizophreniaR37MH043784 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEWIS, DAVID A · 2001 to 2010
$6.8M
NIGMS NIH HHS T32 GM008208NIMH NIH HHS P50 MH103204NIMH NIH HHS R01 MH043784NIMH NIH HHS R37 MH043784
6 · The paper itself

Abstract

Certain clinical features of schizophrenia, such as working memory disturbances, appear to emerge from altered gamma oscillatory activity in the prefrontal cortex (PFC). Given the essential role of GABA neurotransmission in both working memory and gamma oscillations, understanding the cellular substrate for their disturbances in schizophrenia requires evidence from in vivo neuroimaging studies, which provide a means to link markers of GABA neurotransmission to gamma oscillations and working memory, and from postmortem studies, which provide insight into GABA neurotransmission at molecular and cellular levels of resolution. Here, we review findings from both types of studies which converge on the notions that 1) inhibitory GABA signaling in the PFC, especially between parvalbumin positive GABAergic basket cells and excitatory pyramidal cells, is required for gamma oscillatory activity and working memory function; and 2) disturbances in this signaling contribute to altered gamma oscillations and working memory in schizophrenia. Because the PFC is only one node in a distributed cortical network that mediates working memory, we also review evidence of GABA abnormalities in other cortical regions in schizophrenia.

Indexed as

AnimalsCerebral CortexCognitionGABAergic NeuronsHumansInterneuronsMemory, Short-TermModels, NeurologicalSchizophreniaSynaptic TransmissionCognitionGABAInterneuronsNeuroimagingSchizophreniaWorking memory

Identifiers

PMID29936230
PMCPMC6309598

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Registered trials

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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.