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含有β2链的层粘连蛋白调节中枢神经系统突触的精确组织。

Laminins containing the beta2 chain modulate the precise organization of CNS synapses.

作者信息

Egles Christophe, Claudepierre Thomas, Manglapus Mary K, Champliaud Marie-France, Brunken William J, Hunter Dale D

机构信息

Department of Neuroscience, Tufts Center for Vision Research, Boston, MA 02111, USA.

出版信息

Mol Cell Neurosci. 2007 Mar;34(3):288-98. doi: 10.1016/j.mcn.2006.11.004. Epub 2006 Dec 26.

Abstract

Synapses are formed and stabilized by concerted interactions of pre-, intra-, and post-synaptic components; however, the precise nature of the intrasynaptic components in the CNS remains obscure. Potential intrasynaptic components include extracellular matrix molecules such as laminins; here, we isolate beta2-containing laminins, including perhaps laminins 13 (alpha3beta2gamma3) and 14 (alpha4beta2gamma3), from CNS synaptosomes suggesting a role for these molecules in synaptic organization. Indeed, hippocampal synapses that form in vivo in the absence of these laminins are malformed at the ultrastructural level and this malformation is replicated in synapses formed in vitro, where laminins are provided largely by the post-synaptic neuron. This recapitulation of the in vivo function of laminins in vitro suggests that the malformations are a direct consequence of the removal of laminins from the synapse. Together, these results support a role for neuronal laminins in the structural integrity of central synapses.

摘要

突触是由突触前、突触内和突触后成分的协同相互作用形成并稳定的;然而,中枢神经系统中突触内成分的确切性质仍不清楚。潜在的突触内成分包括细胞外基质分子,如层粘连蛋白;在这里,我们从中枢神经系统突触体中分离出含β2的层粘连蛋白,包括可能的层粘连蛋白13(α3β2γ3)和14(α4β2γ3),这表明这些分子在突触组织中发挥作用。事实上,在体内缺乏这些层粘连蛋白的情况下形成的海马突触在超微结构水平上是畸形的,并且这种畸形在体外形成的突触中也会重现,在体外,层粘连蛋白主要由突触后神经元提供。层粘连蛋白在体外对体内功能的这种重现表明,畸形是从突触中去除层粘连蛋白的直接后果。总之,这些结果支持神经元层粘连蛋白在中枢突触结构完整性中的作用。

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