Evidence map›Paper›PMID 31089192›Full record

ReviewMolecular psychiatry2019

Excitation-inhibition balance as a framework for investigating mechanisms in neuropsychiatric disorders.

Vikaas S Sohal, John L R Rubenstein

Open access · greenAbstract readReview
In one paragraph

Review in Molecular psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 592 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
592citing papers in PubMed, 3 pooled it
49.5field-weighted citation impact, top 1% 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

592 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,003 citations in OpenAlex.

  1. Pooled it
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  10. Excitation-inhibition imbalance links amyloid pathophysiology to cognition in non-demented individuals.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  19. Elevation of HNeuroscience bulletin · 2026
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532 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 at 1 institution in 1 country.

Vikaas S SohalDepartment of Psychiatry, Weill Institute for Neurosciences, and Kavli Institute for Fundamental Neuroscience, University of California San Francisco, San Francisco, CA, 94143, USA. vikaas.sohal@ucsf.edu.
John L R RubensteinDepartment of Psychiatry, Weill Institute for Neurosciences, and Kavli Institute for Fundamental Neuroscience, University of California San Francisco, San Francisco, CA, 94143, USA. John.Rubenstein@ucsf.edu.
University of California, San Francisco · US

Funding

Genetic Control of Basal Telencephalic DevelopmentR01MH081880 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 2009 to 2023
$8.1M
Genetic Regulation of Telencephalon DevelopmentR37MH049428 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 2008 to 2017
$5.9M
STRUCTURE, EXPRESSION &FUNCTION OF THE DLX GENE FAMILYR01MH049428 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 1992 to 2022
$5.8M
GENETIC STUDIES OF CORTEX STRUCTURE AND DEVELOPMENTR01NS034661 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 1996 to 2015
$4.6M
Cellular and synaptic mechanisms for dopaminergic modulation of prefrontal cortexR01MH100292 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SOHAL, VIKAAS SINGH · 2013 to 2017
$2.5M
Restoring cognition by optogenetically rescuing gamma rhythms in PFC interneuronsR01MH106507 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SOHAL, VIKAAS SINGH · 2015 to 2019
$2.0M
NIMH NIH HHS R01 MH049428NIMH NIH HHS R01 MH081880NIMH NIH HHS R01 MH100292NIMH NIH HHS R01 MH106507NIMH NIH HHS R37 MH049428NINDS NIH HHS R01 NS034661
6 · The paper itself

Abstract

In 2003 Rubenstein and Merzenich hypothesized that some forms of Autism (ASD) might be caused by a reduction in signal-to-noise in key neural circuits, which could be the result of changes in excitatory-inhibitory (E-I) balance. Here, we have clarified the concept of E-I balance, and updated the original hypothesis in light of the field's increasingly sophisticated understanding of neuronal circuits. We discuss how specific developmental mechanisms, which reduce inhibition, affect cortical and hippocampal functions. After describing how mutations of some ASD genes disrupt inhibition in mice, we close by suggesting that E-I balance represents an organizing framework for understanding findings related to pathophysiology and for identifying appropriate treatments.

Indexed as

AnimalsAutism Spectrum DisorderBrainDisease Models, AnimalHippocampusHumansInhibition, PsychologicalMental DisordersMiceNerve NetNeurons

Identifiers

PMID31089192
PMCPMC6742424
OpenAlexW2945129130

What OpenQuestion holds

Textmetadata
LicenceTDM
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.