Abstract
The neuroplasticity hypothesis is becoming more common in the pathology of depression, however the mechanisms by which stress causes atrophy of neuronal processes and decreases the synapse number is unknown. Here we showed that psychological stress is sensed by the innate immune system in the brain via NLRP3 inflammasome, which in turn releases pro-inflammatory cytokines. The NLRP3 inflammasome has become the focus of a wide range of medical research areas because it is a critical sensor for diverse diseases. Thus, it is critical for the development of new pharmacotherapeutic approaches that target neuro-inflammation in depression.