Status epilepticus induces time-dependent neuronal and astrocytic expression of interleukin-1 receptor type I in the rat limbic system
Status epilepticus induces time-dependent neuronal and astrocytic expression of interleukin-1 receptor type I in the rat limbic system
复制标题
DOI:
10.1016/j.neuroscience.2005.07.063
复制
发表时间:
2006-01-01
期刊:
影响因子:
3.3
通讯作者:
Vezzani, A
中科院分区:
文献类型:
--
作者:
Ravizza, T;Vezzani, A
Interleukin-10 is rapidly synthesized by glia after the induction of seizures. Recent evidence shows that endogenous IL-1 beta has proconvulsant actions mediated by interleukin-1 receptor type I. This receptor also mediates interleukin-1 13 effects on neuronal susceptibility to neurotoxic insults.In this study, we investigated the basal and seizure-induced expression of interleukin-1 receptor type I in rat forebrain to identify the cells targeted by interleukin-1 beta during epileptic activity.Self-sustained limbic status epilepticus was induced in rats by electrical stimulation of the ventral hippocampus. Interleukin-1 receptor type I immunoreactivity was barely detectable in neurons in control brain tissue. During status epilepticus, interleukin-1 receptor type I was induced in the hippocampal neurons firstly, and several hours later in astrocytes localized in limbic and extralimbic areas. Neuronal interleukin-1 receptor type I expression in the hippocampus outlasted the duration of spontaneous electroencephalographic seizure and was not observed in degenerating neurons. Astrocytic expression occurred transiently, between six and 18 h after the induction of status epilepticus and was invariably found in regions of neuronal damage.These time-dependent, cell- and region-specific changes in interleukin-1 receptor type I expression during status epilepticus suggest that interleukin-1 receptor type I in neurons mediates interieukin-1 beta-induced fast changes in hippocampal excitability while interleukin-1 receptor type I receptors in astrocytes may mediate interleukin-1 beta effects on neuronal survival in hostile conditions. (c) 2005 IBRO. Published by Elsevier Ltd. All rights reserved.