Perinatal anoxia/hypoxia is considered a serious risk factor for normal brain development. Anoxia induced by repeated asphyxia at 2 and 4 days after birth resulted in a transient hyperactivity in the small open-field, and a behavioural depression in adult open-field activity of male Wistar rats. The same treatment impaired adult learning behaviour in pole-jumping conditioned avoidance and appetitively motivated hole-board test situations. The calcium entry blocker nimodipine (in doses of 3 and 10 mg/kg) prevented the anoxia-induced changes in orientation motility in the open-field tests and almost fully antagonized the learning deficit in the hole-board test. The behavioural deficit seen during acquisition of the pole-jumping conditioned avoidance response was ameliorated to a lesser degree. The results indicate that the maintenance of calcium homeostasis during the early postnatal phase of brain development is crucial to prevent anoxia-induced behavioural abnormalities.