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首页> 外文期刊>The European Journal of Neuroscience >AAV-mediated delivery of BDNF augments neurogenesis in the normal and quinolinic acid-lesioned adult rat brain.
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AAV-mediated delivery of BDNF augments neurogenesis in the normal and quinolinic acid-lesioned adult rat brain.

机译：AAV介导的BDNF传递增强了正常和喹啉酸损伤的成年大鼠大脑中的神经发生。

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摘要

Brain-derived neurotrophic factor (BDNF) plays a major role in regulating the survival and fate of progenitor cells in the adult brain. In order to extend previous observations in the normal adult brain and advance our knowledge regarding the effect of BDNF on neurogenesis in the injured brain, this study directly compared the effect of BDNF on basal and injury-induced neurogenesis in relation to progenitor cell distribution and levels of neuronal differentiation and survival. BDNF was overexpressed in the subventricular zone (SVZ) via recombinant adeno-associated virus (AAV(1/2)) delivery, and newly generated cells were identified using bromodeoxyuridine (BrdU) labelling. Selective striatal cell loss was induced in a subgroup of rats by unilateral striatal injection of quinolinic acid (QA) 21 days after AAV(1/2) injection. In the normal brain, BDNF overexpression significantly increased BrdU-positive cell numbers in the rostral migratory stream, indicating enhanced progenitor cell migration. FollowingQA lesioning, we observed a reduction in BrdU immunoreactivity in the SVZ. Overexpression of BDNF restored BrdU-positive cell numbers in the QA-lesioned SVZ to that observed in the normal brain. Most significantly, BDNF enhanced the recruitment of progenitor cells to the QA-lesioned striatum and promoted neuronal differentiation in both the normal and QA-lesioned striatum. Our findings indicate that BDNF augments the recruitment, neuronal differentiation and survival of progenitor cells in both neurogenic and non-neurogenic regions of the normal or QA-lesioned brain. Enhanced expression of BDNF may therefore be a viable strategy for augmenting neurogenesis from endogenous progenitor cells.
机译：脑源性神经营养因子（BDNF）在调节成年脑中祖细胞的存活和命运方面起着重要作用。为了扩展先前在正常成人大脑中的观察结果，并增进我们对BDNF对受伤脑神经发生的影响的认识，本研究直接比较了BDNF对基底细胞和损伤诱导的神经发生与祖细胞分布和水平相关的影响。神经元的分化和存活。 BDNF通过重组腺相关病毒（AAV（1/2））传递在脑室下区域（SVZ）中过表达，并使用溴脱氧尿苷（BrdU）标记鉴定了新产生的细胞。 AAV（1/2）注射后21天，通过单侧纹状体注射喹啉酸（QA）在大鼠亚组中诱导选择性纹状体细胞损失。在正常的大脑中，BDNF的过表达显着增加了浮游候鸟流中BrdU阳性细胞的数量，表明祖细胞迁移增加。 QA损伤后，我们观察到SVZ中BrdU免疫反应性降低。 BDNF的过表达使QA损伤的SVZ中的BrdU阳性细胞数恢复到正常大脑中观察到的数。最重要的是，BDNF增强了祖细胞向QA受损纹状体的募集，并促进了正常和QA病变纹状体的神经元分化。我们的发现表明，BDNF可以增强正常或QA病变大脑的神经源性和非神经源性区域中祖细胞的募集，神经元分化和存活。因此，BDNF的增强表达可能是增强内源性祖细胞神经发生的可行策略。

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