Increased neuronal apoptosis in medial prefrontal cortex is accompanied with changes of Bcl-2 and Bax in a rat model of post-traumatic stress disorder.

Post-traumatic stress disorder (PTSD) is an anxiety disorder caused by traumatic experience, which affects a patient's quality of life and social stability. The objective of this study was to determine the apoptosis-related genes B-cell lymphoma 2 (Bcl-2) and BCL2-associated X (Bax) expressions and medial prefrontal cortex (mPFC) neuronal apoptosis after PTSD in rat model and therefore to provide experimental evidence to reveal PTSD pathogenesis. The single-prolonged stress (SPS) method was used to set up the rat PTSD models. Chemiluminescence was used to determine serum corticosterone levels. Neuronal apoptosis was detected using transmission electron microscopy, Hoechst staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Immunohistochemistry, immunofluorescence, RT-PCR, and Western blot were used to detect the expressions of Bcl-2 and Bax protein in mPFC. Our results showed an increased mPFC neuronal apoptosis after SPS stimulation. The number of apoptotic cells peaked on day 7. The expressions of Bcl-2 and Bax peaked on days 4 and 7. The Bcl-2/Bax ratio elevated on days 1 and 4 but decreased markedly on day 7. These results indicated that SPS stimulation increased the number of apoptotic neurons, up-regulated the expressions of Bcl-2 and Bax, and altered the Bcl-2/Bax ratio in the mPFC of PTSD rats.