Role of phosphorylated ERK in amygdala neuronal apoptosis in single-prolonged stress rats.

Studies have shown that single-prolonged stress (SPS) can induce the apoptotic process in the amygdala. In the present study, we aimed to detect expression of phosphorylated p44/42 extracellular signal-regulated kinase (pERK1/2) and apoptosis-related Bax and Bcl-2 and apoptotic cell death in the amygdala region in SPS rats as well as the relation between pERK1/2 and apoptosis. A total of 75 male Wistar rats were randomly divided into control, SPS and PD98059-SPS groups. Rats in the SPS and PD98059-SPS groups were treated with the SPS procedure and were injected with solvent or PD98059 (an inhibitor of ERK), respectively, into the amygdala 30 min before exposure to SPS. The expression of pERK1/2 was detected using immunohistochemistry and Western blotting. The expression of Bax and Bcl-2 was detected using Western blotting and RT-PCR; TUNEL-staining was employed for the detection of apoptotic cells in the amygdala. The results showed that the expression of pERK1/2, the ratio of Bax/Bcl-2 and the TUNEL-positive cell rate significantly increased in the SPS group. After the rats were infused with PD98059, these indices were abolished. In the SPS rat brain, we found that the apoptotic process in the amygdala region was induced by pERK1/2, and this may be related to the abnormal function of the amygdala in post-traumatic stress disorder.