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Postsynaptic TrkB signaling has distinct roles in spine maintenance in adult visual cortex and hippocampus

机译:突触后TrkB信号在成人视觉皮层和海马的脊柱维持中具有独特的作用

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摘要

In adult primary visual cortex (V1), dendritic spines are more persistent than during development. Brain-derived neurotrophic factor (BDNF) increases synaptic strength, and its levels rise during cortical development. We therefore asked whether postsynaptic BDNF signaling through its receptor TrkB regulates spine persistence in adult V1. This question has been difficult to address because most methods used to alter TrkB signaling in vivo affect cortical development or cannot distinguish between pre- and postsynaptic mechanisms. We circumvented these problems by employing transgenic mice expressing a dominant negative TrkB-EGFP fusion protein in sparse pyramidal neurons of the adult neocortex and hippocampus, producing a Golgi-staining-like pattern. In adult V1, expression of dominant negative TrkB-EGFP resulted in reduced mushroom spine maintenance and synaptic efficacy, accompanied by an increase in long and thin spines and filopodia. In contrast, mushroom spine maintenance was unaffected in CA1, indicating that TrkB plays fundamentally different roles in structural plasticity in these brain areas.
机译:在成人初级视觉皮层(V1)中,树突棘比发育期间更持久。脑源性神经营养因子(BDNF)增强突触强度,其水平在皮质发育过程中升高。因此,我们询问是否通过其受体TrkB的突触后BDNF信号传导调节成年V1的脊柱持续性。这个问题很难解决,因为大多数用于体内改变TrkB信号转导的方法会影响皮层发育或无法区分突触前和突触后机制。我们通过使用在成年新皮层和海马的稀疏锥体神经元中表达显性负TrkB-EGFP融合蛋白的转基因小鼠,来产生这些高尔基染色样模式,从而规避了这些问题。在成年V1中,显性阴性TrkB-EGFP的表达导致蘑菇脊椎维持减少和突触效力降低,同时长而细的棘和丝状伪足增加。相反,在CA1中蘑菇脊椎的维护并不受影响,这表明TrkB在这些大脑区域的结构可塑性中起着根本不同的作用。

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