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首页> 外文期刊>Neuron >In vivo restoration of physiological levels of truncated TrkB.T1 receptor rescues neuronal cell death in a trisomic mouse model.
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In vivo restoration of physiological levels of truncated TrkB.T1 receptor rescues neuronal cell death in a trisomic mouse model.

机译：体内恢复截断的TrkB.T1受体的生理水平可以挽救三体小鼠模型中的神经元细胞死亡。

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摘要

Imbalances in neurotrophins or their high-affinity Trk receptors have long been reported in neurodegenerative diseases. However, a molecular link between these gene products and neuronal cell death has not been established. In the trisomy 16 (Ts16) mouse there is increased apoptosis in the cortex, and hippocampal neurons undergo accelerated cell death that cannot be rescued by administration of brain-derived neurotrophic factor (BDNF). Ts16 neurons have normal levels of the TrkB tyrosine kinase receptor but an upregulation of the TrkB.T1 truncated receptor isoform. Here we show that restoration of the physiological level of the TrkB.T1 receptor by gene targeting rescues Ts16 cortical cell and hippocampal neuronal death. Moreover, it corrects resting Ca2+ levels and restores BDNF-induced intracellular signaling mediated by full-length TrkB in Ts16 hippocampal neurons. These data provide a direct link between neuronal cell death and abnormalities in Trk neurotrophin receptor levels.
机译：长期以来，在神经退行性疾病中已有神经营养蛋白或其高亲和力Trk受体失衡的报道。但是，这些基因产物和神经元细胞死亡之间的分子联系尚未建立。在三体性16（Ts16）小鼠中，皮层中的凋亡增加，海马神经元经历加速的细胞死亡，而施用脑源性神经营养因子（BDNF）无法挽救该死亡。 Ts16神经元的TrkB酪氨酸激酶受体水平正常，但TrkB.T1截短的受体亚型上调。在这里，我们显示通过基因靶向恢复TrkB.T1受体的生理水平可以拯救Ts16皮质细胞和海马神经元死亡。此外，它可纠正静息Ca2 +水平并恢复由Ts16海马神经元中全长TrkB介导的BDNF诱导的细胞内信号传导。这些数据提供了神经元细胞死亡与Trk神经营养蛋白受体水平异常之间的直接联系。

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