Activation of ERK by spontaneous seizures in neural progenitors of the dentate gyrus in a mouse model of epilepsy.
Activation of ERK by spontaneous seizures in neural progenitors of the dentate gyrus in a mouse model of epilepsy.
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DOI：
10.1016/j.expneurol.2010.03.003
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发表时间：
2010-07
影响因子：
5.3
通讯作者：
Houser, Carolyn R.
中科院分区：
文献类型：
--
作者：
Li, Yi;Peng, Zechun;Xiao, Bo;Houser, Carolyn R.
关键词：
与颞叶癫痫的自发性发作相关的细胞变化还不清楚，但可能影响正在进行的癫痫相关过程。为了鉴定在自发性癫痫发作时可能发生的细胞信号传导事件，在检测到自发性癫痫发作后以非常短的间隔（1.5-2.5分钟）在癫痫的毛果芸香碱小鼠模型中研究磷酸化细胞外信号调节激酶（pERK）的定位。在海马结构内，pERK的免疫标记在齿状回颗粒下区（SGZ）的细胞亚群中是明显的。这些细胞中的许多细胞具有长的垂直突起，类似于放射状胶质细胞，而另一些细胞具有短突起，并且水平取向。用一系列发育标记物标记表明，几乎所有pERK标记的细胞都是神经祖细胞（NPC）。高百分比（~80%）的pERK标记的细胞被胶质细胞酸性蛋白或脑脂质结合蛋白标记，表明这些细胞是放射状胶质样NPC。标记细胞中表达NeuroD的比例较小，这表明它们后来发展出具有神经元身份的NPC。未成熟神经元中未检测到pERK的早期表达。增殖标记物的双标记表明，约30%的pERK标记的NPC表达Mcm 2，表明它们正在积极增殖。此外，几乎所有处于增殖周期的放射状胶质样NPC都表达pERK。这些发现表明，自发性癫痫发作和相关的ERK激活可能有助于放射状胶质样NPC在这个癫痫模型中的增殖。
Cellular changes that are associated with spontaneous seizures in temporal lobe epilepsy are not well understood but could influence ongoing epilepsy-related processes. In order to identify cell signaling events that could occur at the time of spontaneous seizures, the localization of phosphorylated extracellular signal-regulated kinase (pERK) was studied in a pilocarpine mouse model of epilepsy at very short intervals (1.5-2.5 min) after detection of a spontaneous seizure. Within the hippocampal formation, immunolabeling of pERK was evident in a subpopulation of cells in the subgranular zone (SGZ) of the dentate gyrus at these short intervals. Many of these cells had a long vertical process and resembled radial glia, while others had short processes and were oriented horizontally. Labeling with a series of developmental markers demonstrated that virtually all pERK-labeled cells were neural progenitor cells (NPCs). A high percentage (~80%) of the pERK-labeled cells was labeled with either glial fibrillary acidic protein or brain lipid binding protein, indicating that these cells were radial glia-like NPCs. A smaller percentage of labeled cells expressed NeuroD, suggesting that they were later developing NPCs that were assuming a neuronal identity. Early expression of pERK was not detected in immature neurons. Double labeling with proliferation markers demonstrated that approximately 30% of pERK-labeled NPCs expressed Mcm2, indicating that they were actively proliferating. Furthermore, virtually all radial glia-like NPCs that were in the proliferative cycle expressed pERK. These findings suggest that spontaneous seizures and associated ERK activation could contribute to the proliferation of radial glia-like NPCs in this epilepsy model.
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影响因子：
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通讯作者：
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作者：
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