γ-Aminobutyric Acid-Type A Receptor Deficits Cause Hypothalamic-Pituitary-Adrenal Axis Hyperactivity and Antidepressant Drug Sensitivity Reminiscent of Melancholic Forms of Depression
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Background The gamma-aminobutyric acid (GABA) Type A receptor deficits that are induced by global or forebrain-specific heterozygous inactivation of the gamma2 subunit gene in mouse embryos result in behavior indicative of trait anxiety and depressive states. By contrast, a comparable deficit that is delayed to adolescence is without these behavioral consequences. Here we characterized gamma2-deficient mice with respect to hypothalamic-pituitary-adrenal (HPA) axis abnormalities and antidepressant drug responses.Methods We analyzed the behavioral responses of gamma2(+/-) mice to desipramine and fluoxetine in novelty suppressed feeding, forced swim, tail suspension, and sucrose consumption tests as well as GABA(A) receptor deficit- and antidepressant drug treatment-induced alterations in serum corticosterone.Results Baseline corticosterone concentrations in adult gamma2-deficient mice were elevated independent of whether the genetic lesion was induced during embryogenesis or delayed to adolescence. However, the manifestation of anxious-depressive behavior in different gamma2-deficient mouse lines was correlated with early onset HPA axis hyperactivity during postnatal development. Chronic but not subchronic treatment of gamma2(+/-) mice with fluoxetine or desipramine normalized anxiety-like behavior in the novelty suppressed feeding test. Moreover, desipramine had antidepressant-like effects in that it normalized HPA axis function and depression-related behavior of gamma2(+/-) mice in the forced swim, tail suspension, and sucrose consumption tests. By contrast, fluoxetine was ineffective as an antidepressant and failed to normalize HPA axis function.Conclusions Developmental deficits in GABAergic inhibition in the forebrain cause behavioral and endocrine abnormalities and selective antidepressant drug responsiveness indicative of anxious-depressive disorders such as melancholic depression, which are frequently characterized by HPA axis hyperactivity and greater efficacy of desipramine versus fluoxetine.
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Global heterozygous knockdown of the γ2 subunit leads to anxiety- and despair-like behavior.
“Global heterozygous knockdown of the γ2 subunit leads to impaired GABAergic signaling [11 ], as well as anxiety- and despair-like behavior that is reversed with chronic desipramine (but not fluoxetine) [127] and acute ketamine [126] treatment.”
From An emerging circuit pharmacology of GABAA receptors (2018) · cites this paper as [127]
Anxiety- and despair-like behavior in γ2 knockdown mice is reversed with chronic desipramine but not fluoxetine.
“Global heterozygous knockdown of the γ2 subunit leads to impaired GABAergic signaling [11 ], as well as anxiety- and despair-like behavior that is reversed with chronic desipramine (but not fluoxetine) [127] and acute ketamine [126] treatment.”
From An emerging circuit pharmacology of GABAA receptors (2018) · cites this paper as [127]
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Antidepressant-like properties of α2-containing GABAA receptors
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- Authors
- Shen, Q., Lal, R., Luellen, B. A., Earnheart, J. C., Andrews, A. M., & Luscher, B.
- Affiliations
- Pennsylvania State University (US)
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2010-09
- Volume
- 68
- Issue
- 6
- Pages
- 512-520
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC2930197
- OpenAlex
- W1987472752
- Cited by
- 139
- References
- 74
- Citations by year
- 2026: 6 · 2025: 2 · 2024: 3 · 2023: 8 · 2022: 7 · 2021: 14 · 2020: 6 · 2019: 13 · 2018: 8 · 2017: 7 · 2016: 9 · 2015: 6 · 2014: 6 · 2013: 9 · 2012: 16
- FWCI
- 5.94
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Mental Health (MH62391)
- Pennsylvania Department of Health (MH60989)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- GABAA receptor, hypothalamic-pituitary-adrenal axis, HPA axis hyperactivity, corticosterone, antidepressant sensitivity, desipramine, fluoxetine, endogenous depression, anxiety-like behavior, depression-like behavior, GABAergic inhibition
- MeSH terms
- Animals, Antidepressive Agents, Behavior, Animal, Corticosterone, Depressive Disorder, Desipramine, Disease Models, Animal, Female, Fluoxetine, Hypothalamo-Hypophyseal System, Pituitary-Adrenal System, Receptors, GABA-A, Selective Serotonin Reuptake Inhibitors, Mice, Knockout, Adrenergic Uptake Inhibitors, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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