Abstract
Newborn mammals, showing reduced normal body temperature, might be protected against iron-mediated, delayed neurotoxicity of perinatal asphyxia. Therefore, we investigated the effects of (1) neonatal body temperature and neonatal critical anoxia as well as (2) postanoxic chelation of iron with deferoxamine, on open-field stress-induced behaviour in juvenile rats. The third aim of this study was to compare (after the above-mentioned treatments) circadian changes in spontaneous motor activity and body temperature in juvenile rats permanently protected from any stress. Neonatal anoxia at body temperature adjusted (both during anoxia and 2 h reoxygenation) to a level typical of healthy (37 °C) or febrile (39 °C) adults led to the stress-induced hyperactivity in juvenile (5–45 days old) rats. Both normal neonatal body temperature of 33 °C and chelation of iron prevented the hyperactivity in rats. Neither neonatal body temperature nor neonatal anoxia affected spontaneous motor activity or body temperature of juvenile rats, recorded in their home-cages with implantable transmitters. Circadian rhythmicity was also undisturbed. Presented data support the hypothesis that physiologically reduced neonatal body temperature can provide a protection against iron-mediated postanoxic disturbances of behavioural stress responses in juvenile rats.
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