OBJECTIVETo 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.

METHODSThe 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).

RESULTSThe 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).

CONCLUSIONSThe 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.