幼鼠癫痫持续状态后海马BDNF和TrkB的表达。

Osaka city medical journal Pub Date : 2007-12-01
Toshiaki Yokoi, Daisuke Tokuhara, Mika Saito, Hiroyuki Ichiba, Tsunekazu Yamano
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引用次数: 0

摘要

背景:未成熟的大脑比成熟的大脑更容易发生癫痫发作,但不易发生癫痫引起的神经元丢失。我们通过海马脑源性神经营养因子(BDNF)和酪氨酸激酶B受体(TrkB)的表达,研究了大鼠对卡因酸诱导的癫痫持续状态(KASE)的年龄相关易感性和易感性。方法:kainic acid (KA)诱导癫痫持续状态(SE)后进行免疫组化和Western分析。结果:诱导SE所需的KA剂量从1周龄时的1.5 mg/kg增加到4周龄时的10 mg/kg。SE后,老年大鼠表现出自发性癫痫发作和海马锥体神经元丢失,这与4周龄以下大鼠不同。海马BDNF蛋白表达在1周龄大鼠中增加了5倍,在8周龄大鼠中增加了3倍,在SE后2天恢复到基线。TrkB表达在任何年龄都没有受到KASE的影响。结论:上述结果提示,大鼠SE易感性的关键期为4周龄及以上。由于新生大鼠和成年大鼠BDNF和TrkB对SE的反应模式相似,我们的研究表明,观察到的BDNF的短暂上调不会导致新生大鼠癫痫。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hippocampal BDNF and TrkB expression in young rats after status epilepticus.

Background: The immature brain is more susceptible to seizures than mature brains but less vulnerable to seizure-induced neuronal loss. We studied age-related susceptibility and vulnerability to kainic acid-induced status epilepticus (KASE) in rats in terms of hippocampal expression of brain-derived neurotrophic factor (BDNF) and tyrosine kinase B receptor (TrkB).

Methods: Immunohistochemical and Western analysis were performed after kainic acid (KA)-induced status epilepticus (SE).

Results: KA doses required to induce SE increased from 1.5 mg/kg in 1-week-old rats to 10 mg/kg at 4 weeks of older. After SE the older rats showed spontaneous seizures and hippocampal pyramidal neuronal loss-unlike rats under 4 weeks old. Hippocampal BDNF protein expression had increased fivefold in 1-week-old rats and threefold in 8-week-old rats 1 day after SE, returning to baseline 2 days after SE. TrkB expression showed little effect from KASE at either age.

Conclusions: These results indicated that the critical period as for vulnerability to SE was the age of 4-week-old and older in the rat. Since the response patterns of BDNF and TrkB to SE were similar between neonatal and the adult rats, our study revealed that the observed transient upregulation of BDNF did not contribute to cause epilepsy in neonatal rats.

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