Lipopolysaccharide-induced febrile convulsions in the rat: Short-term sequelae
Lipopolysaccharide-induced febrile convulsions in the rat: Short-term sequelae
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DOI：
10.1111/j.0013-9580.2004.13704.x
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发表时间：
2004-11-01
期刊：
影响因子：
5.6
通讯作者：
Pittman, QJ
中科院分区：
文献类型：
--
作者：
Heida, JG;Boiss, L;Pittman, QJ
目的：热性惊厥（FC）发生在儿童中，由于发烧。FC发生的机制及其对大脑发育的长期影响仍不清楚。我们已经开发了一个模型的FC，通过使用发热作为参数，以测试的假设，发热可以降低癫痫发作阈值和检查的神经系统后遗症的FCs.Methods：14日龄的大鼠幼崽配备体温遥测装置表现出类似的1.5degreesC发热后脂多糖（大肠杆菌，200 /tg/kg）。在这种发热期间，同时给予通常亚惊厥剂量的红藻氨酸用于诱导惊厥伴发热。然后在不同时间处死动物进行病理学和免疫组化研究。结果：配对的脂多糖和亚惊厥红藻氨酸导致惊厥相似的50%的发热动物，死亡率非常低。为了研究这些FC的神经相关性，我们使用了Fos免疫组织化学，发现患有FC的动物在癫痫发作所涉及的脑区域具有Fos阳性免疫反应性。一段时间后的72小时，我们还检查了大脑的病理变化，发现我们groups.Conclusions之间没有差异：我们的数据表明，神经免疫的挑战，其伴随的发热降低癫痫发作阈值。此外，在该模型中，发热诱导的FC对大脑没有短期的不良影响。此外，该模型，通过纳入生理性发热，可能是有用的研究发热及其组成介质的FC的发生中的作用。
Purpose: Febrile convulsions (FCs) occur in children as a result of fever. The mechanisms involved in the genesis of FCs and their long-term consequences on brain development remain unclear. We have developed a model of FC, by using fever as a parameter, to test the hypothesis that fever can lower seizure threshold and to examine the neurologic sequelae of FCs.Methods: Fourteen-day-old rat pups equipped with body-temperature telemetry devices exhibited similar to 1.5degreesC fevers after lipopolysaccharide (Escherichia coli, 200 /tg/kg). During such fevers, concurrently administered doses of kainic acid that are normally subconvulsant were used to induce convulsions with fever. Animals were then killed at varying times for pathological and immunohistochemical studies.Results: The pairing of lipopolysaccharide and subconvulsant kainic acid resulted in convulsions in similar to50% of febrile animals, with very low mortality. To study the neural correlates of these FCs, we used fos immunohistochemistry and found that animals with FCs had fos-positive immunoreactivity in brain regions involved in seizures. After a period of 72 h, we also examined brains for pathologic changes and found no differences among our groups.Conclusions: Our data indicate that a neuroimmune challenge and its accompanying fever reduce the seizure threshold. Furthermore, the FCs induced by fever in this model do not have short-term adverse effects on the brain. In addition, this model, by incorporating physiologic fever, may be useful for examining the role of fever and its constituent mediators in the genesis of FCs.