BDNF regulates the expression of fragile X mental retardation protein mRNA in the hippocampus
BDNF regulates the expression of fragile X mental retardation protein mRNA in the hippocampus
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DOI：
10.1006/nbdi.2002.0544
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发表时间：
2002-10-01
影响因子：
6.1
通讯作者：
Castrén, E
中科院分区：
文献类型：
--
作者：
Castrén, M;Lampinen, KE;Castrén, E
脆性X智力低下蛋白（FMRP）和脑源性神经营养因子（BDNF）都与神经元的成熟和高级认知功能有关。我们已经研究了FMRP和BDNF是否在神经元中受到转录调控。培养的海马神经元暴露于BDNF，而不是NT-3，FMR 1 mRNA水平降低到84.8%的控制在4小时，水平回到基线的24小时或4天。此外，在体内过表达TrkB受体的转基因小鼠的海马中，FMR 1 mRNA的表达降低（对照的82.4%），并且还检测到FMRP蛋白水平的小但显著的降低（5.1%）。相反，与野生型小鼠相比，FMRP缺陷小鼠中BDNF和TrkB mRNA的表达模式没有改变。我们的数据提供了证据，BDNF通过TrkB信号降低FMRP的表达，并建议在BDNF诱导的突触可塑性的FMRP的作用。(C)2002 Elsevier Science（美国）。
Both fragile X mental retardation protein (FMRP) and brain-derived neurotrophic factor (BDNF) are implicated in the maturation of neurons and in the higher cognitive functions. We have investigated whether FMRP and BDNF are reciprocally regulated in neurons. Exposure of cultured hippocampal neurons to BDNF, but not to NT-3, reduced FMR1 mRNA levels to 84.8% of control at 4 h and the levels were back to baseline by 24 h or 4 days. Furthermore, expression of FMR1 mRNA was reduced (82.4% of control) in vivo in the hippocampus of transgenic mice overexpressing TrkB receptors, and a small but significant (5.1%) decrease was also detected in FMRP protein levels. In contrast, the expression patterns of BDNF and TrkB mRNAs were not altered in FMRP-deficient mice compared to wild-type mice. Our data provide evidence that BDNF via TrkB signaling decreases FMRP expression and suggest a role for FMRP in BDNF-induced synaptic plasticity. (C) 2002 Elsevier Science (USA).