Role of the amygdala and MARCKSL1 in anxiety disorders

Abstract

Anxiety disorders are the primary cause of psychiatric disorders in any age group and impose a high socioeconomic burden on modern society. Exposure to severe stress often induces chronic anxiety, which is accompanied by hyperactivation of the hypothalamic-pituitary-adrenal axis, a key regulator for stress response. Currently, no effective therapeutic strategies are able to fully restore neurological function. This is partly due to the complexity of neural circuits associated with anxiety-related behaviors, making it difficult to elucidate the precise pathogenesis of anxiety disorders. Neural dysfunction within the amygdala is associated with anxiety-induced changes in other brain regions, which could have been facilitated by modulation resulting from actin cytoskeletal regulators such as myristoylated alanine-rich C-kinase substrate like 1 (MARCKSL1). Previous reports have indicated that MARCKSL1 transgenic mice, or those exposed to brain injury, exhibited anxiety-like behaviors due to upregulation of MARCKSL1. Moreover, research suggests that attenuation of MARCKSL1 ameliorates anxiety-related behaviors. This review article discusses the amygdala's key role in the mechanism underlying anxiety disorders, with specific focus on MARCKSL1 function.