Single prolonged stress induces dysfunction of endoplasmic reticulum in a rat model of post-traumatic stress disorder.

The aim of the present study, was to investigate the involvement of the endoplasmic reticulum (ER) in post-traumatic stress disorder (PTSD) by detecting changes of ER chaperone protein 78 and ER-resident caspase 12 in the basolateral amygdala after exposure to single prolonged stress (SPS). The established rat model of PTSD was generated by exposure of the animals to SPS. The expression of glucose-regulated protein 78 (GRP78) was examined by immunofluorescence, western blot and reverse transcription-polymerase chain reaction (RT-PCR), and the expression of caspase 12 was examined by western blot and RT-PCR. The morphological changes of the ER were detected by transmission electron microscopy. The results showed that GRP78 expression significantly increased when compared to that in the control group 1 day after SPS exposure (P<0.05). The expression of caspase 12 was also significantly upregulated after SPS exposure and peaked at 7 days following SPS (P<0.05). Morphological evaluation showed that a tumescent ER, ER vacuolization and degranulation of the ER were present following SPS. In conclusion, the findings of the present study suggested that SPS induced GRP78 and caspase 12 upregulation and morphological changes of the ER in the amygdala, which may play important roles in the pathogenesis of PTSD rats.