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首页> 外文期刊>The European Journal of Neuroscience >Differential effects of pro-BDNF on sensory neurons after sciatic nerve transection in neonatal rats.
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Differential effects of pro-BDNF on sensory neurons after sciatic nerve transection in neonatal rats.

机译：前BDNF对新生大鼠坐骨神经横断后感觉神经元的差异作用。

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摘要

Brain-derived neurotrophic factor (BDNF) plays a critical role in the development of the central and peripheral nervous systems, and also in neuronal survival after injury. The actions of BDNF are mediated by its high-affinity receptors TrkB and p75NTR. Recent studies have shown that proneurotrophins bind p75NTR and sortilin with high affinity, and trigger apoptosis of neurons in vitro. As proneurotrophins are a dominant form of gene products in developing and adult animals, it is imperative to understand their physiological functions in animals. Here, we showed differential roles of proBDNF in injured and uninjured sensory neurons. proBDNF, p75NTR and sortilin are highly expressed in dorsal root ganglia (DRG) neurons. Recombinant proBDNF induced a dose-dependent death of PC12 cells and the death activity was completely abolished in the presence of antibodies against the prodomain of BDNF. The exogenous proBDNF enhanced the death of axotomized sensory neurons and the neutralizing antibodies to the prodomain or exogenous sortilin-extracellular domain-Fc fusion molecule reduced the death of axotomized sensory neurons. Interestingly, the treatment of neutralizing antibody in vivo increased the number of sensory neurons in the contralateral DRG. We conclude that proBDNF may induce the death of axotomized sensory neurons and suppress neuronal addition in the intact DRG in neonatal rats, and the suppression of endogenous proBDNF may protect neurons after neurotrauma.
机译：脑源性神经营养因子（BDNF）在中枢神经系统和周围神经系统的发育以及损伤后神经元的存活中起着至关重要的作用。 BDNF的作用由其高亲和力受体TrkB和p75NTR介导。最近的研究表明，神经营养因子以高亲和力结合p75NTR和sortilin，并在体外触发神经元的凋亡。由于神经营养因子是发育中和成年动物中基因产物的主要形式，因此必须了解它们在动物中的生理功能。在这里，我们显示了proBDNF在受伤和未受伤的感觉神经元中的不同作用。 proBDNF，p75NTR和sortilin在背根神经节（DRG）神经元中高度表达。重组proBDNF诱导PC12细胞的剂量依赖性死亡，并且在针对BDNF前域的抗体存在下，死亡活性被完全消除。外源性proBDNF增加了轴突切除的感觉神经元的死亡，并且针对原结构域或外源性sortilin-胞外域-Fc融合分子的中和抗体减少了轴突切除的感觉神经元的死亡。有趣的是，体内中和抗体的治疗增加了对侧DRG中感觉神经元的数量。我们得出的结论是，proBDNF可能诱导新生大鼠完整切除的DRG中轴突切除的感觉神经元的死亡并抑制神经元的添加，而内源性proBDNF的抑制可以保护神经外伤后的神经元。

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