Poststroke subgranular and rostral subventricular zone proliferation in a mouse model of neonatal stroke.
Poststroke subgranular and rostral subventricular zone proliferation in a mouse model of neonatal stroke.
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DOI：
10.1002/jnr.22109
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发表时间：
2009-09
影响因子：
4.2
通讯作者：
Comi, A. M.
中科院分区：
文献类型：
--
作者：
Kadam, S. D.;Mulholland, J. D.;McDonald, J. W.;Comi, A. M.
新生儿脑中风是神经系统发病的一个尚未得到充分研究的原因。最近，我们描述了一种新的未成熟中风小鼠模型，仅利用单侧颈动脉结扎在出生后第 12 天 (P12) CD-1 小鼠中产生梗塞和急性癫痫发作。在这项研究中，在缺血（DAI）后7、14和21天检查了齿状回颗粒下区（SGZ）和室下区（SVZ）的中风后神经祖细胞增殖量。在灌注固定标记新生细胞前 2 小时，单次腹膜内注射（50 毫克/千克）溴脱氧尿苷 (BrdU)。通过与 GFAP、巢蛋白和 DCX 共标记来量化早期细胞表型。对照小鼠显示，神经增殖存在年龄依赖性下降，在 SGZ 和 SVZ 中，与 P19 相比，P33 时 BrdU 标记的细胞计数下降了约 50%。结扎小鼠同侧受损 SGZ 中神经增殖量的显着减少与中风损伤的严重程度和急性癫痫发作评分相关。对侧未检测到类似的相关性。对侧 SGZ 神经增殖最初在 7 DAI 时降低，但在 21 DAI 时恢复正常。在受伤和对照大脑中，约 90% 的新生 SGZ 细胞与巢蛋白共同标记，约 30% 与 GFAP 共同标记，少数与 DCX 共同标记。相反，在 7 DAI 时，中风后 SVZ 细胞增殖同侧比对侧增强。在 SVZ 中，增强的神经增殖通过 P33 正常化至对照水平。总之，新生儿中风后 SGZ 与 SVZ 的神经细胞增殖发生了差异性改变。
Stroke in the neonatal brain is an understudied cause of neurologic morbidity. Recently we have characterized a new immature mouse model of stroke utilizing unilateral carotid ligation alone to produce infarcts and acute seizures in postnatal day 12 (P12) CD-1 mice. In this study, the amount of poststroke neural progenitor proliferation was examined in the subgranular (SGZ) of the dentate gyrus and the subventricular zone (SVZ) 7, 14, and 21 days after ischemia (DAI). A single IP injection (50 mg/kg) of bromodeoxyuridine (BrdU) given 2 hr before perfusion fixation labeled newborn cells. Early cell pheno-types were quantified by colabeling with GFAP, nestin, and DCX. Control mice revealed an age-dependent decrease in neural proliferation, with an ~50% drop in BrdU-labeled cell counts at P33 compared with P19 both in the SGZ and in the SVZ. Significant reduction in the amount of neural proliferation in the ipsilateral injured SGZ of ligated mice correlated with both the severity of the stroke-injury and the acute seizure scores. Similar correlations were not detected contralaterally. Contralateral SGZ neural proliferation was initially lowered at 7 DAI but normalized by 21 DAI. In both injured and control brains, ~90% of newborn SGZ cells colabeled with nestin, ~30% colabeled with GFAP, and a few colabeled with DCX. In contrast, poststroke SVZ cell proliferation was enhanced ipsi- more than contralaterally at 7 DAI. In the SVZ, the enhanced neural proliferation normalized to control levels by P33. In conclusion, the neural cell proliferation was differentially altered in the SGZ vs. SVZ after neonatal stroke.
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