Single-Prolonged Stress Induces Apoptosis by Activating Cytochrome C/Caspase-9 Pathway in a Rat Model of Post-traumatic Stress Disorder

The purpose of this study was to provide a novel insight into the mechanism of how amygdala might participate in PTSD by investigating the changes of cytochrome c oxidase (COX), caspase-9, and caspase-3 in the amygdala of single-prolonged stress (SPS) rats. A total of 80 healthy, male Wistar rats were selected for this study. The models of post-traumatic stress disorder (PTSD) were created by SPS, which is an established animal model for PTSD. The change of COX was detected by light microscope and transmission electron microscopy (TEM). The expression of caspase-9 and caspase-3 in the basolateral amygdala was examined by immunofluorescence and reverse transcription-polymerase chain reaction (RT-PCR). SPS exposure resulted in a significant change of COX in the SPS model groups compared with the normal control group. Evaluation by enzymohistochemistry indicated translocation of COX from mitochondria to cytoplasm. The expression of both caspase-9 and caspase-3 significantly increased 1 day after SPS stimulation, then gradually increased and peaked at SPS 7d. This findings suggest changes of COX, caspase-9, and caspase-3 in the amygdala of SPS rats, which may play important roles in the pathogenesis of PTSD.