缺氧缺血性脑损伤后新生小鼠海马中的BrdU阳性细胞。,BMC Neuroscience

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缺氧缺血性脑损伤后新生小鼠海马中的BrdU阳性细胞。
BMC Neuroscience ( IF 2.4 ) Pub Date : 2005-03-04 , DOI: 10.1186/1471-2202-6-15
John Bartley ₁ , Thomas Soltau , Hereward Wimborne , Sunjun Kim , Angeline Martin-Studdard , David Hess , William Hill , Jennifer Waller , James Carroll

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背景技术尚未完全阐明影响胎儿和新生儿缺氧缺血性（HI）脑损伤的恢复的机制。产时窒息的发生率约为2.5％，但不良临床结局的发生率要低得多。可能导致这种相对良好结果的因素之一是神经发生过程，这已在成年动物中进行了描述。我们使用新生小鼠模型评估HI损伤后海马中的新细胞。结果新生小鼠在出生后第七天进行永久性单侧颈动脉结扎，然后在8％的缺氧环境中暴露75分钟。通过溴脱氧尿嘧啶核苷（BrdU）掺入细胞中并间隔一定时间杀死动物来确定新细胞的存在。结合神经元，神经胶质，内皮和小胶质细胞斑。我们发现，与未受伤的区域相比，受伤区域的新生小鼠海马中BrdU阳性细胞显着增加，在齿状回（DG）中最为明显（154.5 +/- 59.6 v。92.9 +/- 32.7 at受伤后3天；受伤后35天为68.9 +/- 23.4 v。52.4 +/- 17.1，p <0.0011）。在显示分化的细胞中，染色为小胶质细胞或内皮细胞的细胞在DG受伤后三天（受伤侧与未受伤侧相比）显示出峰值增加（30.5 +/- 17.8 v。2.7 +/- 2.6 ，p ＜0.0002）。与成年动物一样，受伤的DG中神经发生显着增加（受伤后35天时为15.0 +/- 4.6 v。5.2 +/- 1.6，p <0.0002），这种增加是在其他动物出现之后分裂细胞。未受伤一侧的DG中新的少突胶质细胞的数量显着更高（7.0 +/- 24.2 v。0.1 +/- 0.3，p <0.0002），这表明受损的海马体少突胶质细胞的合成减少了。结论这些发现表明，新生动物对成年动物的脑损伤具有神经发生反应。此外，HI损伤比单独的缺氧导致更多的神经发生。此过程可能在HI损伤新生动物的恢复中发挥作用，如果这样，增强过程可以改善恢复。结论这些发现表明，新生动物对成年动物的脑损伤具有神经发生反应。此外，HI损伤比单独的缺氧导致更多的神经发生。此过程可能在HI损伤新生动物的恢复中发挥作用，如果这样，增强过程可以改善恢复。结论这些发现表明，新生动物对成年动物的脑损伤具有神经发生反应。此外，HI损伤比单独的缺氧导致更多的神经发生。此过程可能在HI损伤新生动物的恢复中发挥作用，如果这样，增强过程可以改善恢复。

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BrdU-positive cells in the neonatal mouse hippocampus following hypoxic-ischemic brain injury.

BACKGROUND Mechanisms that affect recovery from fetal and neonatal hypoxic-ischemic (H-I) brain injury have not been fully elucidated. The incidence of intrapartum asphyxia is approximately 2.5%, but the occurrence of adverse clinical outcome is much lower. One of the factors which may account for this relatively good outcome is the process of neurogenesis, which has been described in adult animals. We used a neonatal mouse model to assess new cells in the hippocampus after H-I injury. RESULTS Neonatal mice underwent permanent unilateral carotid ligation on the seventh postnatal day followed by exposure to 8% hypoxia for 75 minutes. The presence of new cells was determined by bromodeoxyuridine (BrdU) incorporation into cells with sacrifice of the animals at intervals. Brain sections were stained for BrdU in combination with neuronal, glial, endothelial and microglial stains. We found a significant increase in BrdU-positive cells in the neonatal mouse hippocampus in the injured area compared to the non-injured area, most prominent in the dentate gyrus (DG) (154.5 +/- 59.6 v. 92.9 +/- 32.7 at 3 days after injury; 68.9 +/- 23.4 v. 52.4 +/- 17.1 at 35 days after injury, p < 0.0011). Among the cells which showed differentiation, those which were stained as either microglial or endothelial cells showed a peak increase at three days after the injury in the DG, injured versus non-injured side (30.5 +/- 17.8 v. 2.7 +/- 2.6, p < 0.0002). As in the adult animal, neurogenesis was significantly increased in the DG with injury (15.0 +/- 4.6 v. 5.2 +/- 1.6 at 35 days after injury, p < 0.0002), and this increase was subsequent to the appearance of the other dividing cells. Numbers of new oligodendrocytes were significantly higher in the DG on the non-injured side (7.0 +/- 24.2 v. 0.1 +/- 0.3, p < 0.0002), suggesting that oligodendrocyte synthesis was reduced in the injured hippocampus. CONCLUSION These findings demonstrate that the neonatal animal responds to brain injury with neurogenesis, much like the adult animal. In addition, H-I insult leads to more neurogenesis than hypoxia alone. This process may play a role in the recovery of the neonatal animal from H-I insult, and if so, enhancement of the process may improve recovery.

更新日期：2019-11-01

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