INTRODUCTION: The neuronal cell death associated with perinatal anoxia plays a significant role in neonatal morbidity and neurodevelopmental disability. In response to mild stress, a number of compensatory mechanisms are activated, which allows the cells to survive. Beside decreased body temperature, brain-derived neurotrophic factor (BDNF) is also considered to be beneficial to neuronal survival. AIM(S): Therefore, the aim of this study was to determine whether body temperature under anoxic condition affects the ability of BDNF (proBDNF and mBDNF) to decrease caspase‑3 levels in the developing brain. METHOD(S): 2-day-old Wistar rats were divided into 3 temperature groups: i) normothermic ‑33°C (typical body temperature of newborn rats), ii) hyperthermic – 37°C (typical body temperature of adult rat), and iii) extremely hyperthermic – 39°C (typical body temperature of febrile adult rats). The temperature was controlled starting 15 minutes before, and the measurement was continued during 10 minutes of anoxia (pure nitrogen atmosphere), as well as, for 2 hours postanoxia. Levels of BDNF and caspase-3 were determined post mortem, 2 and 72 hours after anoxia using Western blot and ELISA analysis. RESULTS: Body temperature affected the levels of endogenous BDNF, its precursor form (proBDNF), and caspase‑3. In anoxic animals, the levels of proBDNF and caspase-3 increased with increasing neonatal body temperature. In contrast, a significant negative correlation between the total BDNF to proBDNF ratio, and caspase-3 concentrations was observed. CONCLUSIONS: The results suggest that decreased body temperature can not only up-regulate BDNF levels, but also may affect the other functions of this neuropeptide. FINANCIAL SUPPORT: Research on this paper was supported by grant from National Science Centre, Poland, no. 016/21/N/NZ7/00399.