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新生大鼠全脑缺氧后海马增殖的延迟增加。

A delayed increase in hippocampal proliferation following global asphyxia in the neonatal rat.

作者信息

Scheepens Arjan, Wassink Guido, Piersma Marrit J, Van de Berg Wilma D J, Blanco Carlos E

机构信息

Department of Pediatrics, GROW Research Institute, Maastricht, The Netherlands.

出版信息

Brain Res Dev Brain Res. 2003 Apr 14;142(1):67-76. doi: 10.1016/s0165-3806(03)00032-4.

DOI:10.1016/s0165-3806(03)00032-4
PMID:12694945
Abstract

Adult neurogenesis has been shown to be upregulated following a wide variety of brain injury paradigms. During the first weeks of postnatal life there is around 50 fold more neurogenesis occurring than in the adult CNS, yet little is known regarding the effect of neonatal brain injury on this developmental proliferation. We have investigated the effect of a global perinatal birth asphyxia on postnatal proliferation at 2, 5, 8, 11, 15, 21 and 28 days after birth (injury) using a 3H-thymidine tracer study. We found a specific upregulation of proliferation at 5 days after the injury within the injured hippocampus only, with an associated increase in hippocampal mass and without any changes in GFAP content at any timepoint. Perinatal asphyxia did not alter proliferation within the cerebellum, sub ventricular zone, olfactory bulb, cervical or thoracic spinal cord. Similarly, no changes in corticosterone levels were induced by the injury. Since there were no changes in GFAP content we hypothesize that this increased proliferation is likely neurogenetic, similar to what is seen in the adult brain following injury. Further we show that the dramatic increase in corticosterone at the end of the stress hyporesponsive period is not responsible for the equally dramatic decrease in postnatal proliferation within the CNS.

摘要

在多种脑损伤模型中,成年神经发生已被证明会上调。在出生后的头几周,神经发生的数量比成年中枢神经系统多约50倍,但关于新生儿脑损伤对这种发育性增殖的影响却知之甚少。我们使用³H-胸腺嘧啶核苷示踪研究,调查了围产期全脑性出生窒息对出生后(损伤后)第2、5、8、11、15、21和28天增殖的影响。我们发现,仅在损伤后5天,受损海马体内的增殖有特异性上调,同时海马体质量增加,且在任何时间点胶质纤维酸性蛋白(GFAP)含量均无变化。围产期窒息并未改变小脑、脑室下区、嗅球、颈髓或胸髓内的增殖。同样,损伤也未诱导皮质酮水平发生变化。由于GFAP含量没有变化,我们推测这种增殖增加可能是神经源性的,类似于成年脑损伤后所见的情况。此外,我们还表明,应激低反应期结束时皮质酮的急剧增加并非中枢神经系统内出生后增殖同样急剧减少的原因。

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