Research Topic

Stress Disrupts GABA Signaling: Relevance for Stress-Related Psychiatric Disorders

About this Research Topic

Stress can affect the cellular integrity and functioning of our brain. Traumatic or long-term stress can have deleterious effect on neuronal morphology and network functioning of limbic structures. These stress-induced cellular changes are believed to contribute to the development of various stress-related psychiatric disorders like depressive disorders, PTSD, anxiety disorders or schizophrenia.

It is well documented that GABAergic neurons in the hypothalamus regulate the stress-induced activation of the HPA-axis. However, recent studies suggest that GABA signaling is altered in response to stress also in higher brain areas such as the hippocampus or prefrontal cortex. GABAergic interneurons of the archi- and neocortex orchestrate network oscillations that represent distinct functional states. Emerging evidences suggest that stress can alter the functioning of cortical interneurons and by that likely to contribute to the emotional disturbances and cognitive deficits commonly observed in stress-related psychiatric disorders.

From the clinical perspective it is evident that GABA signaling is a key element in the regulation of emotional responses – evoked by stress – because a family of psychoactive drugs (benzodiazepines) act on GABA receptors and by that has anxiolytic effects. GABAergic changes have been documented by numerous in vivo and post mortem studies investigating the pathophysiology of depressive and bipolar disorders or schizophrenia.

The goal of this Research Topic is to bring together experts studying GABA signaling at the molecular, cellular and network levels in stress related conditions either in clinical settings or in animal models for psychiatric disorders. All papers including behavioral or pharmacological studies are welcome from researchers who work on these topics.


Keywords: Animal model, Anxiety, Bipolar disorder, Depressive disorder, Schizophrenia


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Stress can affect the cellular integrity and functioning of our brain. Traumatic or long-term stress can have deleterious effect on neuronal morphology and network functioning of limbic structures. These stress-induced cellular changes are believed to contribute to the development of various stress-related psychiatric disorders like depressive disorders, PTSD, anxiety disorders or schizophrenia.

It is well documented that GABAergic neurons in the hypothalamus regulate the stress-induced activation of the HPA-axis. However, recent studies suggest that GABA signaling is altered in response to stress also in higher brain areas such as the hippocampus or prefrontal cortex. GABAergic interneurons of the archi- and neocortex orchestrate network oscillations that represent distinct functional states. Emerging evidences suggest that stress can alter the functioning of cortical interneurons and by that likely to contribute to the emotional disturbances and cognitive deficits commonly observed in stress-related psychiatric disorders.

From the clinical perspective it is evident that GABA signaling is a key element in the regulation of emotional responses – evoked by stress – because a family of psychoactive drugs (benzodiazepines) act on GABA receptors and by that has anxiolytic effects. GABAergic changes have been documented by numerous in vivo and post mortem studies investigating the pathophysiology of depressive and bipolar disorders or schizophrenia.

The goal of this Research Topic is to bring together experts studying GABA signaling at the molecular, cellular and network levels in stress related conditions either in clinical settings or in animal models for psychiatric disorders. All papers including behavioral or pharmacological studies are welcome from researchers who work on these topics.


Keywords: Animal model, Anxiety, Bipolar disorder, Depressive disorder, Schizophrenia


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

31 March 2018 Abstract
30 November 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

31 March 2018 Abstract
30 November 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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