The subventricular zone in the immature piglet brain: anatomy and exodus of neuroblasts into white matter after traumatic brain injury.
The subventricular zone in the immature piglet brain: anatomy and exodus of neuroblasts into white matter after traumatic brain injury.
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DOI：
10.1159/000369091
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发表时间：
2015
影响因子：
2.9
通讯作者：
Duhaime AC
中科院分区：
文献类型：
--
作者：
Costine BA;Missios S;Taylor SR;McGuone D;Smith CM;Dodge CP;Harris BT;Duhaime AC
刺激脑室下区（SVZ）中的出生后神经发生和神经母细胞向损伤部位的稳健迁移以响应创伤性脑损伤（TBI）在啮齿类动物中已得到证实;然而，尚不清楚出生后神经发生是否在脑回动物TBI后的修复中发挥作用。在这里，我们描述了解剖的SVZ在小猪的第一次，并开始调查的影响，创伤性脑损伤的SVZ架构和白色的问题，神经母细胞的数量。在所有年龄的未成熟检查SVZ包含一个密集的网状网络的神经源性前体细胞（doublecortin +; DCX）定位直接相邻室管膜细胞（心室SVZ; Vsvz）和成神经细胞组织成链，是从心室SVZ（abventricular SVZ; Asvz）不同。虽然SVZ的结构在不同年龄之间是相似的，但Vsvz和Asvz神经母细胞链的面积随着年龄的增长而下降。在PND 14时，白色物质束具有大量的单个神经母细胞。在我们的比例皮质撞击模型中，病变大小随年龄增加而增加。同样，SVZ对损伤的反应也具有年龄依赖性。较年轻的年龄组，持续的比例最小的病变有最大的SVZ面积，进一步增加，对损伤的反应。在4月龄时受伤且病变最大的仔猪中，SVZ不会因损伤而增加。与人类相似，猪具有丰富的脑回和脑回白色物质，这为研究神经母细胞可能沿着这些白色物质束从SVZ迁移到受损皮质提供了独特的平台。在PND 7时受伤的仔猪中，与未受伤的仔猪相比，TBI并未增加白色物质中的神经母细胞总数，但与对侧半球相比，损伤同侧半球的白色物质中的神经母细胞数量更多，发生了再分布。伤后7天，白色物质中不到1%的神经母细胞在伤后2天内出生。这些数据表明，小猪的SVZ与人类婴儿的SVZ具有许多解剖学相似性，并且TBI对SVZ和白色物质中的成神经细胞数量仅具有适度的影响。处于与人类婴儿相同发育阶段的仔猪在白色物质中配备有最大的SVZ和大量的神经母细胞，这可能足以在损伤修复中不显著刺激神经原性机制。它还有待确定，如果神经发生和迁移神经母细胞发挥的作用，在TBI后的修复和/或如果改变正常迁移过程中活跃的出生后人口的大脑区域是有益的物种与脑回。
Stimulation of postnatal neurogenesis in the subventricular zone (SVZ) and robust migration of neuroblasts to the lesion site in response to traumatic brain injury (TBI) is well-established in rodent species; however, it is not yet known if postnatal neurogenesis plays a role in repair after TBI in gyrencephalic species. Here we describe the anatomy of the SVZ in the piglet for the first time and initiate investigation into the effect of TBI on the SVZ architecture and the number of neuroblasts in the white matter. Among all ages of immaturity examined the SVZ contained a dense mesh network of neurogenic precursor cells (doublecortin+; DCX) positioned directly adjacent to the ependymal cells (ventricular SVZ; Vsvz) and neuroblasts organized into chains that were distinct from the ventricular SVZ (abventricular SVZ; Asvz). Though the architecture of the SVZ was similar among ages, the areas of Vsvz and Asvz neuroblast chains declined with age. At PND 14 the white matter tracts have a tremendous number of individual neuroblasts. In our scaled cortical impact model, lesion size increases with age. Similarly, the response of the SVZ to injury was also age-dependent. The younger age groups that sustained the proportionately smallest lesions had the largest SVZ areas that further increased in response to injury. In piglets that were injured at 4 months of age and had the largest lesions, the SVZ did not increase in response to injury. Similar to humans, swine have abundant gyri and gyral white matter providing a unique platform to study neuroblasts potentially migrating from the SVZ to the lesioned cortex along these white matter tracts. In piglets injured at PND7, TBI did not increase the total number of neuroblasts in the white matter compared to uninjured piglets, but redistribution occurred with a greater number of neuroblasts in the white matter of the hemisphere ipsilateral to the injury compared to the contralateral hemisphere. At 7 days post-injury, less than 1% of neuroblasts in the white matter were born in the 2 days following injury. These data show that the SVZ in the piglet shares many anatomical similarities with the SVZ in the human infant, and that TBI had only modest effects on the SVZ and the number of neuroblasts in the white matter. Piglets at an equivalent developmental stage to human infants were equipped with the largest SVZ and a tremendous number of neuroblasts in the white matter, which may be sufficient in lesion repair without dramatic stimulation of neurogenic machinery. It has yet to be determined if neurogenesis and migrating neuroblasts play a role in repair after TBI and/or if alteration of normal migration during active postnatal population of brain regions is beneficial in species with gyrencephalic brains.
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DOI：
10.1098/rspb.1967.0002
发表时间：
1967-01-01
期刊：
PROCEEDINGS OF THE ROYAL SOCIETY SERIES B-BIOLOGICAL SCIENCES
影响因子：
--
作者：
DICKERSON, JW;DOBBING, J
通讯作者：
DOBBING, J
影响因子：
4.1
作者：
Duhaime, AC;Margulies, SS;Raghupathi, R
通讯作者：
Raghupathi, R
DOI：
10.1007/bf01098647
发表时间：
1972-01-01
期刊：
JOURNAL OF NEUROCYTOLOGY
影响因子：
--
作者：
BLAKEMORE, WF;JOLLY, RD
通讯作者：
JOLLY, RD
影响因子：
5.6
作者：
Boer, Karin;Lucassen, Paul J.;Aronica, Eleonora
通讯作者：
Aronica, Eleonora
DOI：
10.1016/j.ijdevneu.2008.04.001
发表时间：
2008-10-01
影响因子：
1.8
作者：
Koob, Andrew O.;Harris, Brent T.;Duhaime, Ann-Christine
通讯作者：
Duhaime, Ann-Christine