The GABAergic deficit hypothesis of major depressive disorder
Open accessAbstract
Increasing evidence points to an association between major depressive disorders (MDDs) and diverse types of GABAergic deficits. In this review, we summarize clinical and preclinical evidence supporting a central and causal role of GABAergic deficits in the etiology of depressive disorders. Studies of depressed patients indicate that MDDs are accompanied by reduced brain concentration of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) and by alterations in the subunit composition of the principal receptors (GABA(A) receptors) mediating GABAergic inhibition. In addition, there is abundant evidence that suggests that GABA has a prominent role in the brain control of stress, the most important vulnerability factor in mood disorders. Furthermore, preclinical evidence suggests that currently used antidepressant drugs (ADs) designed to alter monoaminergic transmission and nonpharmacological therapies may ultimately act to counteract GABAergic deficits. In particular, GABAergic transmission has an important role in the control of hippocampal neurogenesis and neural maturation, which are now established as cellular substrates of most if not all antidepressant therapies. Finally, comparatively modest deficits in GABAergic transmission in GABA(A) receptor-deficient mice are sufficient to cause behavioral, cognitive, neuroanatomical and neuroendocrine phenotypes, as well as AD response characteristics expected of an animal model of MDD. The GABAergic hypothesis of MDD suggests that alterations in GABAergic transmission represent fundamentally important aspects of the etiological sequelae of MDDs that are reversed by monoaminergic AD action.
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GABA is probably centrally involved in hippocampal and medial prefrontal cortex abnormalities in major depressive disorder.
“GABA is also likely centrally involved in hippocampal and mPFC abnormalities in MDD (134).”
From The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology (2019) · cites this paper as [134]
Antidepressants that target the monoaminergic system have been shown to counteract GABAergic abnormalities.
“antidepressants known to target the monoaminergic system have also shown to counteract GABAergic abnormalities (134).”
From The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology (2019) · cites this paper as [134]
Antidepressant treatment or increases in cellular activation reverses disease and stress-induced changes in GABAergic signaling.
“Conversely, antidepressant treatment or increases in cellular activation (through deep brain stimulation or optogenetic/pharmacological manipulations) reverses these disease and stress-induced changes in GABAergic signaling [123-127].”
From An emerging circuit pharmacology of GABAA receptors (2018) · cites this paper as [123]
Decreases in GABA signaling and GABAergic cell types, and alterations in receptor subtypes, are detected in depressed patients and animals exposed to stress.
“Clinical and preclinical studies provide evidence for a GABA hypothesis in depression where decreases in GABA signaling and GABAergic cell types, as well as alterations in receptor subtypes are detected in depressed patients as well as animals exposed to stress (a factor in the development of depression), for a thorough review of these studies see [123].”
From An emerging circuit pharmacology of GABAA receptors (2018) · cites this paper as [123]
There is substantial evidence that P2X7R modulates 5-HT, NA, glutamate, GABA, and NO release, which are mechanisms consistently involved in stress and depression.
“Altogether, there are substantial evidence that P2X7R modulates 5-HT, NA, glutamate, GABA and NO release, which are mechanisms consistently involved in stress and depression [123,129,130].”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [130]
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- Authors
- Luscher, B., Shen, Q., & Sahir, N.
- Affiliations
- Pennsylvania State University (US)
- Venue
- Molecular Psychiatry
- Published
- 2010-11-16
- Volume
- 16
- Issue
- 4
- Pages
- 383-406
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC3412149
- OpenAlex
- W2057823239
- Cited by
- 934
- References
- 394
- Citations by year
- 2026: 73 · 2025: 75 · 2024: 96 · 2023: 80 · 2022: 67 · 2021: 108 · 2020: 62 · 2019: 72 · 2018: 56 · 2017: 50 · 2016: 28 · 2015: 34 · 2014: 42 · 2013: 30 · 2012: 38
- FWCI
- 20.89
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Pennsylvania Department of Health
- National Institute of Mental Health (R01MH099851, MH62391, R01MH060989, R56MH062391, MH60989, R01MH062391, RC1MH089111)
- Topics
- Health Sciences › Medicine › Pharmacology › 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, GABA, GABAA receptor, inhibitory neurotransmission, stress, hippocampal neurogenesis, antidepressant mechanism, monoaminergic transmission, animal models of depression, etiology of depression
- MeSH terms
- Animals, Antidepressive Agents, Brain, Major Depressive Disorder, Disease Models, Animal, gamma-Aminobutyric Acid, Gene Expression Regulation, Humans, Mutation, Risk Factors, Receptors, GABA, Genetic Predisposition to Disease, Mice
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