The incidence of stroke in children is 2.4 per 100,000 person-years and results in long-term motor and cognitive disability. In ischemic stroke, white matter (WM) is frequently injured, but is relatively understudied compared to grey matter injury. Previous research suggests that the cellular response to WM ischemic injury is different at different ages. Little is known about whether WM repair mechanisms differ in children and adults. We utilized a model of focal ischemic WM injury to determine the oligodendrocyte (OL) response to focal WM ischemic injury in juvenile and adult mice. Methods: Juvenile (21-25 days of age) versus adult (2-3 months of age) mice underwent stereotaxic injection of the potent vasoconstrictor N5-(1-iminoethyhl)-L-ornithine (L-NIO) into the lateral corpus callosum (CC). Animals were sacrificed on postoperative day 3 (acute) or 21 (chronic). Cell birth-dating was performed acutely after WM stroke with 5-ethynyl-2-deoxyuridine (EdU) injected intraperitoneally. Immunohistochemistry was performed, as well as stereology, to measure injury volume. The acute oligodendrocyte progenitor cell (OPC) proliferation and the chronic OL cell fate were determined with immunohistochemistry. Compound action potentials were measured in the CC at acute and chronic time points. Results: Acutely WM injury volume was smaller in juveniles. There was significantly greater OPC proliferation in juvenile animals (acute) compared to adults, but newly born OLs did not survive and mature into myelinating cells at chronic time points. In addition, juveniles did not have improved histological or functional recovery when compared to adults. Protecting newly born OPCs is a potential therapeutic target in children with ischemic stroke.

中文翻译：

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青少年和成年小鼠白质中风后少突胶质祖细胞的增殖和命运。

儿童中风的发生率为每100,000人年2.4，导致长期的运动和认知障碍。在缺血性中风中，白质（WM）经常受伤，但与灰质损伤相比，其研究相对较少。先前的研究表明，对WM缺血性损伤的细胞反应在不同年龄是不同的。关于WM修复机制在儿童和成人中是否有所不同，所知甚少。我们利用局灶性缺血性WM损伤的模型来确定少突胶质细胞（OL）对少年和成年小鼠局灶性WM缺血性损伤的反应。方法：将幼年（21-25天龄）对成年（2-3个月大）小鼠进行立体定位，将强效血管收缩剂N5-（1-亚氨基乙基）-L-鸟氨酸（L-NIO）立体定向注射到lateral体外侧（CC）。在术后第3天（急性）或第21天（慢性）处死动物。WM脑卒中后，腹膜内注射5-乙炔基-2-脱氧尿苷（EdU）进行急性细胞约会。进行了免疫组织化学以及体视学，以测量损伤量。用免疫组织化学测定急性少突胶质祖细胞（OPC）的增殖和慢性OL细胞的命运。在急性和慢性时间点在CC中测量复合动作电位。结果：青少年的WM急性损伤量较小。与成年动物相比，幼年动物（急性）的OPC增殖明显更高，但新生的OL在慢性时间点无法存活并成熟为髓鞘细胞。此外，与成年人相比，未成年人的组织学或功能恢复没有改善。