Elliott R C, Black I B, Dreyfus C F
Department of Neuroscience and Cell Biology, University of Medicine and Dentistry, New Jersey/Robert Wood Johnson Medical School, Piscataway, New Jersey, USA.
J Neurosci Res. 2001 Oct 1;66(1):83-8. doi: 10.1002/jnr.1199.
Extensive evidence suggests that BDNF regulates neural function and architecture after depolarization. Expression of BDNF is increased after depolarization, and the ability of BDNF to modulate synaptic function is well documented. To further investigate BDNF signaling after activity, we analyzed the effects of depolarization or BDNF treatment on receptor mRNA expression in cultured basal forebrain neurons. Levels of mRNA coding for the cognate BDNF receptor, trkB, as well as the common neurotrophin receptor, p75, were quantitated simultaneously using a sensitive solution hybridization technique. Depolarization or BDNF treatment increased p75 mRNA expression 94% and 195%, respectively. In contrast, trkB message decreased 23% after depolarization but was unchanged by BDNF treatment. Together, these changes resulted in significant increases in the p75/trkB ratio after depolarization or BDNF treatment that could alter BDNF binding or signal transduction.
大量证据表明，脑源性神经营养因子（BDNF）在去极化后调节神经功能和结构。去极化后BDNF的表达增加，并且BDNF调节突触功能的能力已有充分记录。为了进一步研究活动后BDNF信号传导，我们分析了去极化或BDNF处理对培养的基底前脑神经元中受体mRNA表达的影响。使用灵敏的溶液杂交技术同时定量编码同源BDNF受体trkB以及共同神经营养因子受体p75的mRNA水平。去极化或BDNF处理分别使p75 mRNA表达增加94％和195％。相反，去极化后trkB信息减少了23％，但BDNF处理未使其改变。总之，这些变化导致去极化或BDNF处理后p75/trkB比率显著增加，这可能会改变BDNF的结合或信号转导。
