Objective: To explore changes of neuronal calcium channel following brain damage induced by injection of pertussis bacilli in rats, and to investigate the relationship between cytosolic free calcium concentration ([Ca 2+ ] i) in the synaptosome and Ca 2+ ATPase activities of mitochondria. Methods: The level of [Ca 2+ ] i in the synaptosome and Ca 2+ ATPase activities of mitochondria in the acute brain damage induced by injection of pertussis bacilli (PB) in rat was determined and nimodipine was administrated to show its effects on [Ca 2+ ] i in the synaptosome and on alteration of Ca 2+ ATPase activity in the mitochondria. Seventy three rats were randomly divided into four groups, ie, normal control group (Group A), sham operation control group (Group B), PB group (Group C) and nimodipine treatment group (Group D). Results: The level of [Ca 2+ ] i was significantly increased in the PB injected cerebral hemisphere in the Group C as compared with that in the Group A and the Group B at 30 minutes after injection of PB. The level of [Ca 2+ ] i was kept higher in the 4 hours and 24 hours subgroups after the injection in the Group C (P< 0.05 ). In contrast, the Ca 2+ ATPase activities were decreased remarkably among all of the subgroups in the Group C. Nimodipine, which was administered after injection of PB, could significantly decrease the [Ca 2+ ] i and increase the activity of Ca 2+ ATPase (P< 0.05 ). Conclusions: The neuronal calcium channel is opened after injection of PB. There is a negative correlation between activities of Ca 2+ ATPase and [Ca 2+ ] i. Nimodipine can reduce brain damage through stimulating the activities of Ca 2+ ATPase in the mitochondria, and decrease the level of [Ca 2+ ] i in the synaptosome. Treatment with nimodipine dramatically reduces the effects of brain damage induced by injection of PB. Objective: To explore changes of neuronal calcium channel following brain damage induced by injection of pertussis bacilli in rats, and to investigate the relationship between cytosolic free calcium concentration ([Ca 2+] i) in the synaptosome and Ca 2+ ATPase activities of mitochondria . Methods: The level of [Ca 2+] i in the synaptosome and Ca 2+ ATPase activities of mitochondria in the acute brain damage induced by injection of pertussis bacilli (PB) in rat was determined and nimodipine was administrated to show its effects on [Ca 2+] i in the synaptosome and on alteration of Ca 2+ ATPase activity in the mitochondria. Seventy three rats were randomly divided into four groups, ie, normal control group (Group A), sham operation control group (Group B) , PB group (Group C) and nimodipine treatment group (Group D). Results: The level of [Ca 2+] i was significantly increased in the PB injected cerebral hemisphere in the Group C compare d with that in the Group A and the Group B at 30 minutes after injection of PB. The level of [Ca 2+] i was kept higher in the 4 hours and 24 hours subgroups after the injection in the Group C (P <0.05 ). In contrast, the Ca 2+ ATPase activities were decreased remarkably among all of the subgroups in the Group C. Nimodipine, which was administered after injection of PB, could significantly decrease the [Ca 2+] i and increase the activity of Ca 2+ ATPase (P <0.05). Conclusions: The neuronal calcium channel is opened after injection of PB. There is a negative correlation between activities of Ca 2+ ATPase and [Ca 2+] i. Nimodipine can reduce brain damage through stimulating the activities of Ca 2+ ATPase in the mitochondria, and decrease the level of [Ca 2+] i in the synaptosome. Treatment with nimodipine dramatically reduces the effects of brain damage induced by injection of PB.