Abstract

There is a sex difference in vulnerability to PTSD and in response to therapeutic interventions. Since relation between gonadal hormones and PTSD has been revealed, this study aimed to understand the severity of PTSD-induced impairments after ovarian hormone deficiency and the influence of exercise on PTSD accompanied by ovarian hormone deficiency. Female adult Wistar rats were subjected to ovariectomy, PTSD, or combination ovariectomy plus PTSD. Twenty days after ovariectomy, PTSD was induced by single prolonged stress (SPS) model. The exercise started 14 days after SPS and continued for 4 weeks. Thirty minutes moderate treadmill exercise was planned for 5 days per week. On day 65, after assessing rats using the elevated plus-maze (EPM) test, corticosterone, BDNF, and apoptotic markers were tested. p < 0.05 was considered as significant level. The results showed that ovariectomy worsened the effect of SPS on hippocampal BDNF and led to greater increase in serum corticosterone and hippocampal caspase 3 and BAX in SPS rats. Also, ovariectomy exacerbated anxiety-like behavior in SPS rats. Exercise improved the alterations of hippocampal BDNF, corticosterone, caspase 3, and BAX in SPS ovariectomized rats. However, exercise had no statistically significant effect on anxiety-like behavior in this group. According to the results, exercise is effective to attenuate SPS-induced impairments in molecular and cellular responses even when the condition becomes more complicated due to ovarian hormone deficiency. However, exercise alone cannot help to improve behavior impairments in PTSD combined with an ovarian hormone deficiency. Therefore, exercise could likely be considered as a complementary intervention to strengthen other treatments.

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