The Effect of Pre-Conditioning Endurance Training on Neurogenic and Anti-Neurogenic Factor in Hippocampus of Male Rats Following Ischemic Reperfusion

Binding of mature brain derived neurotrophic factor (BDNF) to tyrosine kinase B (TrkB) receptor leads to cell survival, while proBDNF binding to p75 receptor leads to cell death. Thus the aim of the present study was to investigate the effects of eight weeks pre-conditioning endurance training on BDNF, TrkB, proBDNF and p75 levels in the hippocampus male rats following ischemic reperfusion.

40 male wistar rats (12 weeks old and 236.56 ± 16.98g) were divided into four groups, including: ischemic control, ischemic training, healthy control, healthy training. Training groups (healthy and ischemic), trained with 30m/min (70% VO2max), 30min/day, and 5 days/week for 8 weeks on the treadmill. To induce ischemia (in ischemic groups), carotid artery is clamped with microsurgery clamp for 45 minutes. For data analysis, one-way ANOVA and post hoc Tukey tests were performed at a significance level of P ˂ 0.05.

The results showed that BDNF levels in hippocampus of ischemic control group were significantly lower than healthy control group (P = 0.001). Also BDNF levels in hippocampus of ischemic training group were higher than ischemic control group (P = 0.002). TrkB levels in control group were significantly lower than healthy control group (P = 0.026). But despite increasing in TrkB levels of ischemic training group than ischemic control group wasn’t significant (P = 0.556). proBDNF levels in ischemic control group were significantly higher than healthy control group (P = 0.001). No significant difference were found in proBDNF levels of ischemic training group than ischemic control (P = 0.418). No significant difference were found in p75 levels in difference were found in different group (P = 0.071).

Based on these results, it seems that pre-conditioning endurance training can have neuroprotective effect through improving BDNF, TrkB and proBDNF levels in hippocampus and can prevent apoptosis and neuronal death following ischemic reperfusion and can be studied as a complementary therapy in ischemic disease.