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首页> 外文期刊>The European Journal of Neuroscience >Lack of neurogenesis in the adult rat cerebellum after Purkinje cell degeneration and growth factor infusion.
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Lack of neurogenesis in the adult rat cerebellum after Purkinje cell degeneration and growth factor infusion.

机译：浦肯野细胞变性和生长因子输注后，成年大鼠小脑缺乏神经发生。

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Although constitutive neurogenesis exclusively occurs in restricted regions of the adult mammalian brain, resident progenitors can be isolated from many different CNS sites, and neuronal neogeneration can be stimulated in vivo by injury or infusion of growth factors. To ask whether latent compensatory mechanisms, which may be exploited to promote repair processes, are present throughout the CNS, we examined the neurogenic potentialities of the adult rat cerebellum in normal conditions, following injury, and after infusion of growth factors. Degeneration of Purkinje cells was induced by intracerebroventricular administration of the toxin saporin, conjugated to anti-p75 antibodies. In addition, epidermal growth factor and basic fibroblast growth factor, or FGF8, were infused for 2 weeks to either intact or injured animals. In all conditions, proliferating cells were identified from bromodeoxyuridine (BrdU) incorporation. In the unmanipulated cerebellum there were rare dividing cells, mainly represented by NG2-positive presumptive oligodendrocyte precursors. Mitotic activity was strongly enhanced in cortical areas with Purkinje cell degeneration, being mostly sustained by microglia, plus minor fractions of NG2-expressing cells, astrocytes and oligodendrocytes. In contrast, growth factor infusion had a weak effect on both intact and injured cerebella. In all experimental conditions, we never found any BrdU-positive cells coexpressing distinctive markers for immature or differentiated cerebellar neurons. Therefore, although some progenitor cells reside in the adult cerebellum, the local environment, either intact or injured, does not provide efficient cues to direct their differentiation towards neuronal phenotypes. In addition, neurogenic potentialities cannot be induced or boosted by the application of growth factors which are effective in other CNS regions.
机译：尽管本构神经发生仅发生在成年哺乳动物脑的受限区域，但常驻祖细胞可以从许多不同的中枢神经系统部位分离出来，并且神经元新生可以通过损伤或注入生长因子而在体内被刺激。为了询问在整个中枢神经系统中是否存在潜在的补偿机制（可用于促进修复过程），我们检查了正常情况下，损伤后和输注生长因子后成年大鼠小脑的神经源性潜力。通过脑室内给予与抗p75抗体缀合的毒素saporin诱导浦肯野细胞变性。此外，将表皮生长因子和碱性成纤维细胞生长因子或FGF8注入完整或受伤的动物2周。在所有条件下，从溴脱氧尿苷（BrdU）掺入中鉴定出增殖细胞。在未操纵的小脑中，存在稀少的分裂细胞，主要由NG2阳性的推测性少突胶质细胞前体代表。浦肯野细胞变性可大大增强皮质区域的有丝分裂活性，大部分由小胶质细胞维持，此外还有少量的NG2表达细胞，星形胶质细胞和少突胶质细胞。相比之下，生长因子输注对完整和受伤的小脑均具有较弱的作用。在所有实验条件下，我们从未发现任何BrdU阳性细胞共表达未成熟或分化的小脑神经元的独特标记。因此，尽管某些祖细胞存在于成年小脑中，但完整或受损的局部环境不能提供有效的线索来指导它们向神经元表型的分化。另外，不能通过应用在其他CNS区域中有效的生长因子来诱导或增强神经源性潜力。

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