Neonatal anoxia is an example of early-life threatening experience that might exert long-lasting behavioral disturbance. One of the consequences of neonatal asphyxia is hyperactivity in open-field test. Changes in open-field activity are coupled with changes in the function of the hypothalamic-pituitary-adrenal (HPA) axis. A critical determinant of the severity of hypoxic-ischemic brain injury in newborn rats is body temperature. Hyperthermia under anoxic conditions increases locomotor activity in the open-field test. Therefore, the aim of the present study was to test whether body temperature during neonatal anoxia can affect basal and stress-induced corticosterone secretion in rats. At the age of 2 days Wistar rat pups were exposed to anoxia in 100% nitrogen atmosphere. Rectal temperature was kept at 33 degrees C (typical for the rat pups), or was elevated to a level typical for febrile adults (39 degrees C). Control rats were exposed to atmospheric air under the respective thermal conditions. Basal and stress-induced corticosterone levels were assessed using sulphuric acid-induced fluorescence, on postnatal day 14. Body temperature during neonatal asphyxia altered the early developmental profile of plasma corticosterone. Hyperthermia under anoxic conditions decreased the corticosterone response to open-field stress. In conclusion, febrile body temperature changes corticosterone release, which might induce neurobehavioral disturbances. On the other hand, a protection against the HPA dysfunction can be achieved by the reduced physiological neonatal body temperature.
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