Decreased body temperature during anoxia affects the endogenous BDNF level in tertiary phase of injury

Asphyxia before, during, or after birth is an important cause of perinatal mortality and morbidity. The mechanism underlying neurological damage resulting from anoxia episode is complex and is not limited to the anoxia episode. Although the benefits of therapeutic hypothermia in secondary failure of oxidative metabolism have long been known, the principle of this therapy in tertiary phase of repair and reorganization have not yet to be fully elucidated. Currently brain-derived neurotrophic factor (BDNF) is also considered to be beneficial to neuronal survival. Therefore, our experiments aimed at determining the effects of low body temperature during simulated perinatal anoxia on the level of the neurotrophic brain-derived factor (BDNF) and on the correlation between the level of BDNF (proBDNF and mBDNF) and the level of active caspase-3 (marker of apoptosis) in developing brain in tertiary phase after exposure. The results demonstrated that the ability of BDNF to inhibit caspase-3 activation and subsequent apoptosis likely accounts in large part for its protection against neuronal damage only in rats maintaining the low body temperature.