GABAergic Control of Amygdala: Regulation by Stress and Relevance to Neuropsychiatric Diseases

To promote survival, our brains need to appropriately process the ever-changing events in our living environments. Many of these events, are more or less stressful. Amygdala, a nuclei complex located deep inside the temporal lobe, has emerged as a central hub of stress processing in our brain. One prominent feature which distinguishes amygdala from many of its neighboring regions such as hippocampus and cortex is that the inhibitory tone in this region is particularly high under resting state. Such a highly inhibitory tone, which is primarily sustained by GABAergic interneuronal network, is thought to be prerequisite for our brain to filter most neutral events and prevent us to generate inappropriate emotional and behavioral response to these events. However, when we are exposed to a stressful state, the GABAergic inhibition in amygdala will be quickly removed, which, as a consequence, allows the swift transfer of the stressful information from amygdala to the downstream nuclei in the hypothalamus, middle brain and brainstem to elicit appropriate behavioral and emotional response. As such, dynamic GABAergic regulation in amygdala has constituted one of the kernel neurobiological bases of stress processing in brain. Of note is that several extreme states of stress such as earthquake and wars may cause desregulation of GABAergic inhibition in amygdala, which is generally manifested as persistent loss of GABAergic control of amygdala. Such disinhibition is known to essentially contribute to the development of a spectrum of stress-related neuropsychological diseases such anxiety disorders and depression. Many of the pharmacological therapeutics available for treatment of mental illness have their anxiolytic and/or antidepressant effects partially through augmenting GABAergic inhibition in amygdala.

In this Research Topic, we aim to collect original research articles as well as reviews and perspective articles to 1) provide novel basic and clinical evidence regarding the molecular, synaptic and circuit mechanisms underlying the GABAergic control of amygdala and its regulation/desregulation by stress; 2) find new approaches targeting GABAergic regulation in amygdala to prevent and treat stress-related neuropsychiatric illness.