Cited by 149Treatment of Major DepressionNeuroscience and Neuropharmacology ResearchNeurotransmitter Receptor Influence on Behavior

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GABAergic Control of Depression-Related Brain States

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Luscher, Bernhard, Fuchs, Thomas·2015·Advances in Pharmacology

DOI 10.1016/bs.apha.2014.11.003PMC PMC4784429

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Abstract

The GABAergic deficit hypothesis of major depressive disorders (MDDs) posits that reduced γ-aminobutyric acid (GABA) concentration in brain, impaired function of GABAergic interneurons, altered expression and function of GABA(A) receptors, and changes in GABAergic transmission dictated by altered chloride homeostasis can contribute to the etiology of MDD. Conversely, the hypothesis posits that the efficacy of currently used antidepressants is determined by their ability to enhance GABAergic neurotransmission. We here provide an update for corresponding evidence from studies of patients and preclinical animal models of depression. In addition, we propose an explanation for the continued lack of genetic evidence that explains the considerable heritability of MDD. Lastly, we discuss how alterations in GABAergic transmission are integral to other hypotheses of MDD that emphasize (i) the role of monoaminergic deficits, (ii) stress-based etiologies, (iii) neurotrophic deficits, and (iv) the neurotoxic and neural circuit-impairing consequences of chronic excesses of glutamate. We propose that altered GABAergic transmission serves as a common denominator of MDD that can account for all these other hypotheses and that plays a causal and common role in diverse mechanistic etiologies of depressive brain states and in the mechanism of action of current antidepressant drug therapies.

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Authors: Luscher, B., & Fuchs, T.
Affiliations: Pennsylvania State University (US)
ORCID: Fuchs, Thomas
Venue: Advances in Pharmacology
Publisher: Elsevier
Published: 2015
Volume: 73
Pages: 97-144
ISSN: 1054-3589 (ISSN-L)
DOI: 10.1016/bs.apha.2014.11.003
PMC: PMC4784429
OpenAlex: W135939678
Cited by: 149
References: 329
Citations by year: 2026: 15 · 2025: 12 · 2024: 16 · 2023: 10 · 2022: 9 · 2021: 23 · 2020: 23 · 2019: 18 · 2018: 8 · 2017: 6 · 2016: 8 · 2015: 1
FWCI: 22.97
Type: book chapter
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Advances in pharmacology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Universität Zürich
National Institute of Mental Health (R21MH097247, R01MH099851, R01MH083911, MH099851, MH097247, MH083911, RC1MH089111)
Topics: Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords: major depressive disorder, GABAergic neurotransmission, GABAA receptor, GABAergic interneurons, chloride homeostasis, antidepressant mechanism, glutamate excitotoxicity, neural circuits, animal models of depression
MeSH terms: Animals, Antidepressive Agents, Brain, Major Depressive Disorder, Disease Models, Animal, gamma-Aminobutyric Acid, Humans, Synaptic Transmission, Receptors, GABA-A

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GABAergic Control of Depression-Related Brain States

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