癫痫持续状态导致幼鼠海马体中可逆性神经元损伤：一种标志物的新用途。
Status epilepticus results in reversible neuronal injury in infant rat hippocampus: novel use of a marker.
作者信息
Chang D, Baram T Z
机构信息
Division of Neurology, Childrens Hospital Los Angeles, CA 90027.
出版信息
Brain Res Dev Brain Res. 1994 Jan 14;77(1):133-6. doi: 10.1016/0165-3806(94)90220-8.
Abstract
Despite ready induction of severe limbic status epilepticus by systemic kainic acid (KA) in infant rats, excitotoxic neuronal injury has not been observed. The mechanisms of this resistance of the immature hippocampus to excitotoxicity are unknown. Acid fuchsin stain has been used as a marker of irreversibly injured neurons in the adult brain. We speculated that the dye might map reversibly injured neurons in the infant. Subsequent to KA-induced status epilepticus in 11-day-old rats, acid fuchsin stain was evident in the hippocampal CA3, CA1, dentate gyrus and hilus by 24 h, peaked at 48 h and disappeared by 6 days, without evidence for neuronal loss. Acid fuchsin may be a useful tool for delineating the distribution of reversibly injured immature neurons in experimental seizure paradigms.
摘要
尽管在幼鼠中通过全身注射红藻氨酸（KA）可轻易诱发严重的边缘性癫痫持续状态，但尚未观察到兴奋性毒性神经元损伤。未成熟海马对兴奋性毒性的这种抗性机制尚不清楚。酸性品红染色已被用作成人大脑中不可逆损伤神经元的标志物。我们推测该染料可能标记幼鼠中可逆性损伤的神经元。在11日龄大鼠中KA诱发癫痫持续状态后，酸性品红染色在海马CA3、CA1、齿状回和海马门在24小时时明显可见，在48小时达到峰值，并在6天时消失，且无神经元丢失的证据。酸性品红可能是在实验性癫痫发作模型中描绘可逆性损伤的未成熟神经元分布的有用工具。
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本文引用的文献
1
Continuous c-fos expression precedes programmed cell death in vivo.体内持续的c-fos表达先于程序性细胞死亡。
Nature. 1993 May 13;363(6425):166-9. doi: 10.1038/363166a0.
2
Induction of c-fos mRNA by kindled seizures: complex relationship with neuronal burst firing.点燃性癫痫发作诱导c-fos mRNA表达：与神经元爆发式放电的复杂关系
J Neurosci. 1993 Feb;13(2):744-51. doi: 10.1523/JNEUROSCI.13-02-00744.1993.
3
Kainic acid induced limbic seizures: metabolic, behavioral, electroencephalographic and neuropathological correlates.海人酸诱发的边缘叶癫痫：代谢、行为、脑电图及神经病理学相关性
Brain Res. 1981 Aug 10;218(1-2):299-318. doi: 10.1016/0006-8993(81)91308-1.
4
Fate of the hippocampal mossy fiber projection after destruction of its postsynaptic targets with intraventricular kainic acid.用脑室注射红藻氨酸破坏海马苔藓纤维投射的突触后靶点后其命运
J Comp Neurol. 1981 Mar 10;196(4):549-69. doi: 10.1002/cne.901960404.
5
Kainic acid-induced limbic seizures: electrophysiologic studies.海人酸诱发的边缘叶癫痫发作：电生理学研究
Neurology. 1981 Jul;31(7):806-12. doi: 10.1212/wnl.31.7.806.
6
Minireview. Kainic acid as a tool for the study of temporal lobe epilepsy.
Life Sci. 1981 Nov 16;29(20):2031-42. doi: 10.1016/0024-3205(81)90659-7.
7
Kainic-acid-induced seizures: a developmental study.
Brain Res. 1984 Mar;315(1):139-48. doi: 10.1016/0165-3806(84)90085-3.
8
Maturation of kainic acid seizure-brain damage syndrome in the rat. II. Histopathological sequelae.
Neuroscience. 1984 Dec;13(4):1073-94. doi: 10.1016/0306-4522(84)90289-6.
9
The distribution of hypoglycemic brain damage.低血糖性脑损伤的分布情况。
Acta Neuropathol. 1984;64(3):177-91. doi: 10.1007/BF00688108.
10
Epileptic phenomena produced by kainic acid in laboratory rats during ontogenesis.
Physiol Bohemoslov. 1988;37(5):395-405.
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