Evidence map›Paper›PMID 28697889›Full record

ReviewBiological psychiatry2017

Somatostatin-Positive Gamma-Aminobutyric Acid Interneuron Deficits in Depression: Cortical Microcircuit and Therapeutic Perspectives.

Corey Fee, Mounira Banasr, Etienne Sibille

Abstract readReview
In one paragraph

Review in Biological psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed, 1 pooled it
10.9field-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

189 citing papers in PubMed, 1 synthesis or guideline pooled it, 330 citations in OpenAlex.

  1. Pooled it
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  9. NAcLat-DBS reduces GABANeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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  11. Essential Oils: Chemistry and Mechanisms of Anticonvulsant Action.International journal of molecular sciences · 2026
    Review
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129 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

3 authors at 2 institutions in 1 country.

Corey FeeCampbell Family Mental Health Research Institute of Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada.
Mounira BanasrCampbell Family Mental Health Research Institute of Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada.
Etienne SibilleCampbell Family Mental Health Research Institute of Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada; Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada. Electronic address: etienne.sibille@camh.ca.
University of Toronto · CACentre for Addiction and Mental Health · CA

Funding

Transcriptome analysis in major depressionR01MH077159 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MCCLUNG, COLLEEN A, SIBILLE, ETIENNE L · 2007 to 2015
$3.2M
NIMH NIH HHS R01 MH077159
6 · The paper itself

Abstract

The functional integration of external and internal signals forms the basis of information processing and is essential for higher cognitive functions. This occurs in finely tuned cortical microcircuits whose functions are balanced at the cellular level by excitatory glutamatergic pyramidal neurons and inhibitory gamma-aminobutyric acidergic (GABAergic) interneurons. The balance of excitation and inhibition, from cellular processes to neural network activity, is characteristically disrupted in multiple neuropsychiatric disorders, including major depressive disorder (MDD), bipolar disorder, anxiety disorders, and schizophrenia. Specifically, nearly 3 decades of research demonstrate a role for reduced inhibitory GABA level and function across disorders. In MDD, recent evidence from human postmortem and animal studies suggests a selective vulnerability of GABAergic interneurons that coexpress the neuropeptide somatostatin (SST). Advances in cell type-specific molecular genetics have now helped to elucidate several important roles for SST interneurons in cortical processing (regulation of pyramidal cell excitatory input) and behavioral control (mood and cognition). Here, we review evidence for altered inhibitory function arising from GABAergic deficits across disorders and specifically in MDD. We then focus on properties of the cortical microcircuit, where SST-positive GABAergic interneuron deficits may disrupt functioning in several ways. Finally, we discuss the putative origins of SST cell deficits, as informed by recent research, and implications for therapeutic approaches. We conclude that deficits in SST interneurons represent a contributing cellular pathology and therefore a promising target for normalizing altered inhibitory function in MDD and other disorders with reduced SST cell and GABA functions.

Indexed as

AnimalsAntidepressive AgentsCerebral CortexDepressiongamma-Aminobutyric AcidHumansInterneuronsNerve NetSomatostatinAntidepressive Agentsgamma-Aminobutyric AcidSomatostatinDepressionDimensionalGABAMicrocircuitPathologySomatostatin

Identifiers

PMID28697889
PMCPMC5610074
OpenAlexW2622461305

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.