Inflammation contributes to seizure-induced hippocampal injury in the neonatal rat brain.

Inflammation contributes to seizure-induced hippocampal injury in the neonatal rat brain.
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炎症会导致新生大鼠大脑中癫痫发作引起的海马损伤。

DOI:
10.1111/j.1600-0404.2007.00804.x
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发表时间:
2007
影响因子:
3.5
通讯作者:
Shin,D
Shin,D
中科院分区:
医学3区
文献类型:
--
作者:
Sankar,R;Auvin,S;Mazarati,A;Shin,D

文献摘要

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目的:实验性癫痫持续状态(SE)引起的海马神经元损伤程度与年龄有关,在许多新生儿癫痫发作模型中不易证实。 新生儿癫痫发作通常发生在包括炎症成分的临床环境中。我们研究了潜在的贡献作用预先存在的炎症作为一个重要的变量,在介导neuronal injury.Materials and Methods-出生后第7天(P7)和P14大鼠幼崽注射脂多糖(LPS),2小时前,锂-毛果芸香碱(LiPC)诱导SE。  神经元损伤进行了评估,通过良好的描述histologicmethods.Results -虽然LPS本身并没有产生任何明显的细胞损伤在任何年龄,这种治疗加剧了海马损伤诱导的LiPC-SE。该效果是高度选择性的CA 1 subfield.Conclusions-炎症可以大大有助于未成熟的海马癫痫发作诱导的神经元损伤的脆弱性。 炎症和早期癫痫发作时间延长的综合影响可能会影响新生儿癫痫发作的长期结局。
Objective –The extent of neuronal injury in the hippocampus produced by experimental status epilepticus (SE) is age dependent and is not readily demonstrable in many models of neonatal seizures. Neonatal seizures often occur in clinical settings that include an inflammatory component. We examined the potential contributory role of pre‐existing inflammation as an important variable in mediating neuronal injury.Materials and methods –Postnatal day 7 (P7) and P14 rat pups were injected with lipopolysaccharide (LPS), 2 h prior to SE induced by lithium–pilocarpine (LiPC). Neuronal injury was assessed by well‐described histologic methods.Results –While LPS by itself did not produce any discernible cell injury at either age, this treatment exacerbated hippocampal damage induced by LiPC–SE. The effect was highly selective for the CA1 subfield.Conclusions –Inflammation can contribute substantially to the vulnerability of immature hippocampus to seizure‐induced neuronal injury. The combined effects of inflammation and prolonged seizures in early life may impact long‐term outcomes of neonatal seizures.