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研究了大剂量地塞米松对谷氨酸诱发清醒小鼠和离体小鼠原代培养皮层细胞兴奋毒性损伤的影响。小鼠单侧纹状体灌注谷氨酸单钠（ＭＳＧ）引起纹状体内局灶性损伤，此损伤可被６ｍｇ／ｋｇＭＫ－８０１预防。５０ｍｇ／ｋｇ地塞米松每日腹腔注射使该损伤体积增加约１１０±２４．５％。地塞米松还促进ｄｌ－谷氨酸对小鼠原代培养皮层细胞活性的损伤。大剂量地塞米松增加小鼠脂质过氧化产物ＭＤＡ含量，但不增加小鼠不完全性脑缺血所致ＭＤＡ升高，且明显减轻缺血性谷胱甘肽过氧化物酶活性的抑制。对小鼠皮层分离细胞，３μｍｏｌ地塞米松快速并明显加强谷氨酸诱发的细胞内游离钙升高。结果提示：大剂量糖皮质激素增加神经元兴奋性毒性损伤可能有钙相关的快速效应参与
The effect of high dose dexamethasone on the excitotoxicity of glutamate-induced awake mice and primary cultured cortical cells in vitro was studied. Mouse unilateral striatal perfusion of monosodium glutamate (MSG) causes focal lesions in the striatum, which can be prevented by 6 mg / kg MK-801. Daily intraperitoneal injections of 50 mg / kg dexamethasone increased the lesion volume by about 110 ± 24.5%. Dexamethasone also promotes dl-glutamate on mouse primary cultured cortical cell damage. High-dose dexamethasone increased MDA content in mouse lipid peroxidation products, but did not increase MDA level caused by incomplete cerebral ischemia in mice, and significantly reduced the inhibition of ischemic glutathione peroxidase . For mouse cortical cells, 3 μmol dexamethasone rapidly and significantly enhanced glutamate-induced intracellular free calcium elevation. The results suggest that high doses of glucocorticoids increase the excitotoxicity of neurons may have a rapid calcium-related effects