Quantitative immunochemistry on neuronal loss, reactive gliosis and BBB damage in cortex/striatum and hippocampus/amygdala after systemic kainic acid administration.

Ding M; Haglid KG; Hamberger A

首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Quantitative immunochemistry on neuronal loss, reactive gliosis and BBB damage in cortex/striatum and hippocampus/amygdala after systemic kainic acid administration.

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Quantitative immunochemistry on neuronal loss, reactive gliosis and BBB damage in cortex/striatum and hippocampus/amygdala after systemic kainic acid administration.

机译：全身性海藻酸给药后，皮质/纹状体和海马/杏仁核的神经元丢失，反应性神经胶质细胞增生和BBB损伤的定量免疫化学分析。

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Cell specific markers were quantified in the hippocampus, the amygdala/pyriform cortex, the frontal cerebral cortex and the striatum of the rat brain after systemic administration of kainic acid. Neuron specific enolase (NSE) reflects loss of neurons, glial fibrillary acidic protein (GFAP) reflects reactive gliosis, and brain levels of serum proteins measures blood-brain-barrier permeability. While the concentration of NSE remained unaffected in the frontal cerebral cortex and the striatum, their GFAP content increased during the first three days. In the hippocampus and amygdala, NSE levels decreased significantly. GFAP levels in the hippocampus were unaffected after one day and decreased in the amygdala/pyriform cortex. After that, GFAP increased strikingly until day 9 or, in the case of amygdala/pyriform cortex, even longer. This biphasic time course for GFAP was accompanied by a decrease of S-100 during days 1-9 followed by a significant increase at day 27 above the initial level. The regional differences in GFAP and S-100 could result from the degree of neuronal degeneration, the astrocytic receptor set-up and/or effects on the blood-brain barrier.

机译：全身施用海藻酸后，在海马，杏仁核/梨状皮层，额叶大脑皮层和纹状体中定量细胞特异性标记物。神经元特异性烯醇化酶（NSE）反映了神经元的丧失，神经胶质原纤维酸性蛋白（GFAP）反映了反应性神经胶质增生，血清蛋白的大脑水平衡量了血脑屏障的通透性。虽然NSE的浓度在额叶大脑皮层和纹状体中不受影响，但它们的GFAP含量在前三天内有所增加。在海马和杏仁核中，NSE水平显着下降。一天后，海马中的GFAP水平未受影响，杏仁核/梨形皮质中的GFAP水平下降。此后，GFAP显着增加直至第9天，对于杏仁核/梨形皮层，则持续更长时间。 GFAP的这种双相时程伴随着S-100在第1-9天下降，随后在第27天比初始水平显着上升。 GFAP和S-100的区域差异可能是由于神经元变性程度，星形细胞受体的建立和/或对血脑屏障的影响所致。

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《Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry》 |2000年第5期|共6页
作者
Ding M; Haglid KG; Hamberger A;
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正文语种 eng
中图分类生物化学;
关键词
Blood-Brain Barrier; Excitatory Amino Acid Agonists; Gliosis; Kainic Acid; 血脑屏障; 兴奋性氨基酸激动剂; 神经胶质增生; 红藻氨酸; 神经元;

机译：Blood-Brain Barrier;Excitatory Amino Acid Agonists;Gliosis;Kainic Acid;血脑屏障;兴奋性氨基酸激动剂;神经胶质增生;红藻氨酸;神经元;

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1. Quantitative immunochemistry on neuronal loss, reactive gliosis and BBB damage in cortex/striatum and hippocampus/amygdala after systemic kainic acid administration. [J] . Ding M, Haglid KG, Hamberger A Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry . 2000,第4a5期

机译：全身性海藻酸给药后，皮质/纹状体和海马/杏仁核的神经元丢失，反应性神经胶质细胞增生和BBB损伤的定量免疫化学分析。
2. Folic acid deficiency increases delayed neuronal death, DNA damage, platelet endothelial cell adhesion molecule-1 immunoreactivity, and gliosis in the hippocampus after transient cerebral ischemia. [J] . Hwang IK, Yoo KY, Suh HW, Journal of Neuroscience Research . 2008,第9期

机译：叶酸缺乏会增加短暂性脑缺血后海马迟发性神经元死亡，DNA损伤，血小板内皮细胞粘附分子1免疫反应性和神经胶质增生。
3. The effect of 3-nitropropionic acid on behavioral dysfunction, neuron loss and gliosis in the brain of adult male rats: The case of prefrontal cortex, hippocampus and the cerebellum [J] . Torabi Abolfazl, Joneidi Mohammadjavad, Mohammadzadeh Ibrahim, Toxicon: An International Journal Devoted to the Exchange of Knowledge on the Poisons Derived from Animals, Plants and Microorganisms . 2020,第1期

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4. Ganoderma Lucidum Reduces Kainic Acid-Induced Hippocampal Neuronal Damage via Inflammatory Cytokines and Glial Fibrillary Acid Protein Expression [C] . Aguirre Moreno A.C, Campos Pena V., Villeda Hernez J., Western Pharmacology Society . 2011

机译：灵芝通过炎症细胞因子和胶质纤维酸蛋白表达减少了Kinain酸诱导的海马神经元损伤
5. Inhibition by the adenosine analogue (R-)-N6-phenylisopropyladenosine of kainic acid neurotoxicity in rat hippocampus after systemic administration. [O] . D. G. MacGregor, T. W. Stone 1993

机译：全身给药后腺苷类似物（R-）-N6-苯基异丙基腺苷对大鼠海马的海藻酸神经毒性的抑制作用。
6. Inhibition by the adenosine analogue, (R-)-N6-phenylisopropyladenosine, of kainic acid neurotoxicity in rat hippocampus after systemic administration. [O] . MacGregor, D. G., Stone, T. W. 1993

机译：全身给药后，腺苷类似物（R-）-N6-苯基异丙基腺苷对大鼠海马的海藻酸神经毒性的抑制作用。
7. Systemic Administration of Kainic Acid Increases GABA Levels in Perfusate fromthe Hippocampus of Rats 'In vivo' [R] . Zhang, W. Q., Rogers, B. C., Tandon, P., 1990

机译：全身给予红藻氨酸可增加大鼠体内海马内灌注液中GaBa的水平

Quantitative immunochemistry on neuronal loss, reactive gliosis and BBB damage in cortex/striatum and hippocampus/amygdala after systemic kainic acid administration.

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