摘要
目的研究谷氨酸（Ｇｌｕ）对皮质神经元的损伤及对Ｃａ２＋／ＣａＭＰＫⅡ活性的影响。方法５００μｍｏｌ／ＬＧｌｕ作用１０ｍｉｎ，测Ｃａ２＋／ＣａＭＰＫⅡ及乳酸脱氢酶（ＬＤＨ）活性。结果Ｃａ２＋／ＣａＭＰＫⅡ活性和正常对照相比下降４６．３％，１００μｍｏｌ／Ｌ氯胺酮几乎完全保护该酶活性；ＬＤＨ活性在１ｈ时无明显变化，２４ｈ时明显升高。结论（１）Ｇｌｕ对皮质神经元损伤致Ｃａ２＋／ＣａＭＰＫⅡ活性下降早于ＬＤＨ变化；（２）Ｃａ２＋／ＣａＭＰＫⅡ活性下降主要由ＮＭＤＡ受体介导，与非ＮＭＤＡ受体无关。
Objective To study the effect of glutamate(Glu) on Ca^2+/Calmodulin-dependent protein kinase Ⅱ activity in cultured cortical neurons. Methods The cultured neurons were exposed to 500μmol/L Glu for 10min.The activities of Ca^2+/Calmodulin-dependent protein kinaseⅡ and LDH were assayed.Results Ca2+/Calmodulin-dependent protein kinaseⅡ activity decreased by 46.3% compared with control and 100μmol/L ketamine protected the activity almost completely. The LDH activity showed no singnificant change 1h after treatment, but was singnificantly increased after 24h.Conclusions (1) Glutamate exposure caused delayed neuronal death was preceded by singnificant inhibition of Ca^2+/Calmodulin-dependent protein kinaseⅡ. (2)The inhibition of Ca^2+/Calmodulin-dependent protein kinaseⅡ activity was NMDA receptor mediated, not related to non-NMDA receptors.
出处
《徐州医学院学报》
CAS
1997年第6期3-6,共4页
Acta Academiae Medicinae Xuzhou
基金
国家自然科学基金
