New Insights into the Pivotal Role of the Amygdala in Inflammation-Related Depression and Anxiety Disorder

Depression and anxiety disorders are the two most prevalent psychiatric diseases that affect hundreds of millions of individuals worldwide. Understanding the etiology and related mechanisms is of great importance and might yield new therapeutic strategies to treat these diseases effectively. During the past decades, a growing number of studies have pointed out the importance of the stress-induced inflammatory response in the amygdala, a kernel region for processing emotional stimuli, as a potentially critical contributor to the pathophysiology of depression and anxiety disorders. In this review, we first summarized the recent progress from both animal and human studies toward understanding the causal link between stress-induced inflammation and depression and anxiety disorders, with particular emphasis on findings showing the effect of inflammation on the functional changes in neurons in the amygdala, at levels ranging from molecular signaling, cellular function, synaptic plasticity, and the neural circuit to behavior, as well as their contributions to the pathology of inflammation-related depression and anxiety disorders. Finally, we concluded by discussing some of the difficulties surrounding the current research and propose some issues worth future study in this field.

Automated summary

Depression and anxiety disorders are the most common psychiatric diseases worldwide, and understanding the causal link between stress-induced inflammation and these diseases is crucial for effective treatment. This review summarizes recent progress in animal and human studies, highlighting the impact of stress-induced inflammation on functional changes in amygdala neurons and its contribution to the pathology of depression and anxiety disorders.