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用离体孵育的大鼠海马脑片模型，研究兴奋毒性与Ｃａ２＋／ＣａＭＰＫＩＩ活性的关系。结果表明，外源性谷氨酸或ＮＭＤＡ均可抑制Ｃａ２＋／ＣａＭＰＫＩＩ的活性，此活性的抑制可被ＭＫ８０１完全拮抗，而ＤＮＱＸ却无明显拮抗作用；无胞外Ｃａ２＋时，谷氨酸导致的酶活性抑制程度不如有胞外Ｃａ２＋时显著；无胞外Ｍｇ２＋时，谷氨酸导致的酶活性抑制程度比有胞外Ｍｇ２＋时显著。结果提示兴奋毒性对Ｃａ２＋／ＣａＭＰＫＩＩ活性的抑制与ＮＭＤＡ受体介导的兴奋毒性有关
The rat hippocampal slices incubated in vitro were used to study the relationship between excitotoxicity and Ca2 + / CaMPKII activity. The results showed that exogenous glutamate or NMDA could inhibit the activity of Ca2 + / CaMPKII, the inhibition of this activity can be completely antagonized by MK801, but no significant antagonism of DNQX; no extracellular Ca2 +, glutamate-induced enzyme The degree of inhibition was not as significant as that of extracellular Ca2 +. When extracellular Mg2 + was absent, the inhibitory effect of glutamic acid on enzyme activity was more significant than that of extracellular Mg2 +. The results suggest that the inhibition of Ca2 + / CaMPKII activity by excitotoxicity is related to NMDA receptor-mediated excitotoxicity