Ignatowicz E, Vezzani A M, Rizzi M, D'Incalci M
Laboratory of Cancer Chemotherapy and Neuropharmacology, Istituto di Ricerche Farmacologiche 'Mario Negri', Milano, Italy.
Neuroreport. 1991 Nov;2(11):651-4. doi: 10.1097/00001756-199111000-00004.
We investigated whether in vivo excitotoxicity was mediated by a mechanism of programmed cell death called apoptosis. Neurotoxic doses of kainic acid (1.2 nmol) and quinolinic acid (120 nmol) were unilaterally injected in the dorsal hippocampus of anesthetized rats. Eight or 16 h later the animals were killed and DNA was extracted from the injected hippocampi. DNA from mouse thymocytes exposed to methylprednisolone (10(-5) M for 6 h at 37 degrees C) was used as a positive control of apoptotic cells. No typical 'ladder' of DNA fragments (multimers of approximately 200 Kb) which characterizes apoptosis was seen in hippocampal cells after toxic doses of kainic or quinolinic acid, as assessed by agarose gel electrophoresis. This suggests that hippocampal nerve cell death induced in vivo by the excitotoxins is not mediated by apoptosis.
我们研究了体内兴奋性毒性是否由一种称为凋亡的程序性细胞死亡机制介导。将神经毒性剂量的 kainic 酸（1.2 nmol）和喹啉酸（120 nmol）单侧注射到麻醉大鼠的背侧海马体中。8 或 16 小时后处死动物，并从注射的海马体中提取 DNA。将暴露于甲基强的松龙（10^(-5) M，在 37 摄氏度下作用 6 小时）的小鼠胸腺细胞的 DNA 用作凋亡细胞的阳性对照。通过琼脂糖凝胶电泳评估，在给予毒性剂量的 kainic 酸或喹啉酸后，海马体细胞中未观察到表征凋亡的典型 DNA 片段“梯形”（约 200 Kb 的多聚体）。这表明兴奋性毒素在体内诱导的海马神经细胞死亡不是由凋亡介导的。
