Melancholia with Onset During Treatment with SSRIs

Swartz, Conrad M.; Guadagno, G

doi:10.3109/10401239809147035

Cited by 5 publications

(1 citation statement)

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“…Consistent with our findings in γ2 +/− mice, fluoxetine and TCAs are known to exhibit different effects on HPA axis function in animal models and patients. Fluoxetine increases Cort concentrations in animal models (60) and fails to normalize HPA axis activity in patients (49, 50, 61). In contrast, desipramine and other TCAs normalize HPA axis function in animal models (60, 62, 63) and patients (64), and this drug effect is associated with remission from depression (64, 65).…”

Section: Discussionmentioning

confidence: 99%

γ-Aminobutyric Acid-Type A Receptor Deficits Cause Hypothalamic-Pituitary-Adrenal Axis Hyperactivity and Antidepressant Drug Sensitivity Reminiscent of Melancholic Forms of Depression

Shen

Lal

Luellen

et al. 2010

Biological Psychiatry

131

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BACKGROUND: GABA A receptor deficits that are induced by global or forebrain-specific heterozygous inactivation of the γ2 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 γ2-deficient mice with respect to HPA axis abnormalities and antidepressant drug responses.

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Section: Discussionmentioning

confidence: 99%

γ-Aminobutyric Acid-Type A Receptor Deficits Cause Hypothalamic-Pituitary-Adrenal Axis Hyperactivity and Antidepressant Drug Sensitivity Reminiscent of Melancholic Forms of Depression

Shen

Lal

Luellen

et al. 2010

Biological Psychiatry

131

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GABAergic Control of Depression-Related Brain States

Lüscher

Fuchs

2015

Advances in Pharmacology

118

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The GABAergic deficit hypothesis of major depressive disorders posits that reduced GABA concentration in brain, impaired function of GABAergic interneurons, altered expression and function of GABAA receptors, and changes in GABAergic transmission dictated by altered chloride homeostasis can contribute to the etiology of Major Depressive Disorder (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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An electrophysiological model of major depression: Relevance to clinical subtyping and pharmacological management

Cerda

Fitzgerald

2021

Psychiatry Research

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Melancholia with Onset During Treatment with SSRIs

Cited by 5 publications

References 0 publications

γ-Aminobutyric Acid-Type A Receptor Deficits Cause Hypothalamic-Pituitary-Adrenal Axis Hyperactivity and Antidepressant Drug Sensitivity Reminiscent of Melancholic Forms of Depression

γ-Aminobutyric Acid-Type A Receptor Deficits Cause Hypothalamic-Pituitary-Adrenal Axis Hyperactivity and Antidepressant Drug Sensitivity Reminiscent of Melancholic Forms of Depression

GABAergic Control of Depression-Related Brain States

An electrophysiological model of major depression: Relevance to clinical subtyping and pharmacological management

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