TrkB对发育中的小脑浦肯野细胞突触消除的需求。

Brain cell biology Pub Date : 2006-02-01 Epub Date: 2007-03-01 DOI:10.1007/s11068-006-9002-z
Laurens W J Bosman, Jana Hartmann, Jaroslaw J Barski, Alexandra Lepier, Michael Noll-Hussong, Louis F Reichardt, Arthur Konnerth
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引用次数: 55

摘要

受体酪氨酸激酶TrkB及其配体脑源性神经营养因子(BDNF)和神经营养因子-4/5 (NT-4/5)对中枢神经系统的生长、存活和活动依赖性突触增强至关重要。这些trkb介导的作用以高度细胞类型特异性的方式发生。在这里,我们报道了富含TrkB受体的小脑浦肯野细胞在TrkB缺陷小鼠中发育为正常形态。因此,与其他类型的神经元相比,浦肯野细胞不需要TrkB来促进树突生长和脊柱形成。相反,我们在trkb缺陷小鼠的浦肯野细胞中发现了gaba能突触成熟的适度延迟,更重要的是,在浦肯野细胞中发现了异常的多攀爬纤维神经。因此,我们的研究结果表明TrkB受体参与突触消除,并揭示了受体酪氨酸激酶在大脑中的新作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Requirement of TrkB for synapse elimination in developing cerebellar Purkinje cells.

The receptor tyrosine kinase TrkB and its ligands, brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5), are critically important for growth, survival and activity-dependent synaptic strengthening in the central nervous system. These TrkB-mediated actions occur in a highly cell-type specific manner. Here we report that cerebellar Purkinje cells, which are richly endowed with TrkB receptors, develop a normal morphology in trkB-deficient mice. Thus, in contrast to other types of neurons, Purkinje cells do not need TrkB for dendritic growth and spine formation. Instead, we find a moderate delay in the maturation of GABAergic synapses and, more importantly, an abnormal multiple climbing fiber innervation in Purkinje cells in trkB-deficient mice. Thus, our results demonstrate an involvement of TrkB receptors in synapse elimination and reveal a new role for receptor tyrosine kinases in the brain.

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