[Effect of excitatoxicity on Ca2+/CaM PK II activity in rat hippocampal slices]

The relation between Ca2+/CaM PK II activity and excitatoxicity was studied in an in vitro model of rat hippocampal slices. The slices were exposed to 50-200 mumol.L-1 glutamate or 25-100 mumol.L-1 NMDA and glucose-free Krebs buffer for 30 min after being recovered to normal conditions by 2 hours of incubation with standard Krebs buffer. The results showed that inhibition of Ca2+/CaM PK II activity in rat hippocampal slices was induced by exogenous EAA (glutamate or NMDA), and Ca2+/CaM PK II activity values decreased to 50.1% and 44.7% of control at 200 mumol.L-1 glutamate and 100 mumol.L-1 NMDA, respectively; MK801, but not DNQX, antagonized EAA-induced inhibition of Ca2+/CaM PK II activity. When the slices were pretreated with MK801 prior to exposure to 200 mumol.L-1 glutamate or 100 mumol.L-1 NMDA, the Ca2+/Cam PK II activity values were 91.5% and 96.7%, respectively. The changes of extracellular Ca2+ or Mg2+ concentration influenced Ca2+/CaM PK II activity of the slices exposed to exogenous glutamate; Ca2+/CaM PK II activity values in the presence of extracellular Ca2+ was lower than that in the absence of extracellular Ca2+, and it changed from 50.1% of control (presence of Ca2+) to 64% of control (absence of Ca2+) at 200 mumol.L-1 glutamate, but Ca2+/CaM PK II activity values in the presence of extracellular Mg2+ was higher than that in the absence of extracellular Mg2+, and it changed from 50.1% of control(presence of Mg2+) to 36.6% of control (absence of Mg2+) at 200 mumol.L-1 glutamate. The results suggest that NMDA receptor may be involved in excitotoxicity-induced inhibition of Ca2+/CaM PK II activity.