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首页> 外文期刊>The European Journal of Neuroscience >Dynamic patterns of BDNF expression in injured sensory neurons: differential modulation by NGF and NT-3.
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Dynamic patterns of BDNF expression in injured sensory neurons: differential modulation by NGF and NT-3.

机译：受伤的感觉神经元中BDNF表达的动态模式：NGF和NT-3的差异调节。

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It has been suggested that altered retrograde neurotrophin support contributes to the phenotypic switch observed in BDNF expression in injured sensory neurons. Thus, modulatory influences of NGF and NT-3 on BDNF expression in injured adult rat DRG neurons were examined using in situ hybridization and immunohistochemical approaches. Quantitative analysis reveals a biphasic response to sciatic nerve injury, whereby in the first day following injury, BDNF expression is up-regulated in approximately 83% of injured neurons including all small neurons, and a larger pool of trkB expressing neurons than in intact. By 1 week and up to 3 weeks later expression is still seen in approximately 66% of injured neurons, but the characteristic phenotypic switch in the subpopulations expressing BDNF occurs, whereby expression in the trkA population is reduced and expression in trkB- and in trkC-positive neurons is elevated. NGF infusion results in elevated levels of BDNF expression in both intact and injured trkA-positive neurons, accompanied by reduced trkB expression. NT-3 acts in an opposite fashion effecting a down-regulation in BDNF expression in intact neurons and preventing/reducing the injury-associated increases in BDNF expression in both trkC- and nontrkC-expressing subpopulations of injured neurons. These effects suggest NGF can regulate BDNF expression in trkA-expressing neurons regardless of the axonal state and that elevated levels of BDNF may contribute to the down-regulation in trkB expression associated with these states. Furthermore, the findings demonstrate that NT-3 can act in an antagonistic fashion to NGF in the regulation of BDNF expression in intact neurons, and mitigate BDNF's expression in injured neurons.
机译：已经提出，改变的逆行神经营养因子支持导致在受损的感觉神经元中BDNF表达中观察到的表型转换。因此，使用原位杂交和免疫组织化学方法检查了NGF和NT-3对成年大鼠DRG神经元BDNF表达的调节作用。定量分析揭示了对坐骨神经损伤的双相反应，由此在损伤后的第一天，BDNF表达在大约83％的受损神经元（包括所有小神经元）和大量trkB表达神经元中被完整表达。到1周到3周后，仍然有大约66％的受损神经元表达，但是在表达BDNF的亚群中出现了典型的表型转换，从而减少了trkA群体中的表达，并在trkB-和trkC-中表达。阳性神经元升高。 NGF输注会导致完整和受损的trkA阳性神经元中BDNF表达水平升高，并伴随着trkB表达降低。 NT-3以相反的方式起作用，从而影响完整神经元中BDNF表达的下调，并防止/减少了在受损神经元的trkC和非trkC表达亚群中BDNF表达中与损伤相关的增加。这些效应表明，NGF可以调节表达trkA的神经元中的BDNF表达，而与轴突状态无关，而BDNF的升高水平可能有助于与这些状态相关的trkB表达的下调。此外，该发现表明NT-3可以在调节完整神经元中的BDNF表达中与NGF产生拮抗作用，并减轻受损神经元中BDNF的表达。

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