The downregulation of Autophagy in amygdala is sufficient to alleviate anxiety-like behaviors in Post-traumatic Stress Disorder model mice.

Abstract

Post-traumatic stress disorder (PTSD) is one of the most serious and harmful stress-related emotion disorders resulting from traumatic experiences. Upregulation of autophagic flux in neuronal cells is believed to play a pivotal role in the pathogenesis of PTSD, however, the region-specific effects of autophagy upregulation in PTSD have not been fully investigated. In our study, inhibiting autophagy in the amygdala rather than in the medial prefrontal cortex or hippocampus of wild-type mice alleviated anxiety-like behaviors in a PTSD mouse model. Our results also suggested upregulating autophagic activity in the amygdala reversed the anxiolytic effect observed in Fmr1 knockout mice, which may have resulted from reduced autophagy levels in the brains of these mice. In conclusion, the impact of autophagy on PTSD may be region-dependent, even within PTSD-related neuronal circuits.