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.
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.
