Substantial migration of SVZ cells to the cortex results in the generation of new neurons in the excitotoxically damaged immature rat brain

被引：26

作者：

Faiz, Maryam ^{[1
]}

Acarin, Laia ^{[1
]}

Villapol, Sonia ^{[1
]}

Schulz, Stefan ^{[2
]}

Castellano, Bernardo ^{[1
]}

Gonzalez, Berta ^{[1
]}

机构：

[1] Univ Autonoma Barcelona, Dept Cell Biol Physiol & Immunol, Inst Neurosci, E-08193 Barcelona, Spain

[2] Univ Jena, Inst Pharmakol & Toxikol, D-07743 Jena, Germany

来源：

MOLECULAR AND CELLULAR NEUROSCIENCE | 2008年 / 38卷 / 02期

关键词：

neurogenesis; gliogenesis; CNS injury; differentiation; chemokine; NMDA;

D O I：

10.1016/j.mcn.2008.02.002

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Mammalian SVZ progenitors continuously generate new neurons in the olfactory bulb. After injury, changes in SVZ cell number suggest injury-induced migration. Studies that trace the migration of SVZ precursors into neurodegenerating areas are lacking. Previously, we showed a decrease in BrdU + SVZ cells following excitotoxic damage to the immature rat cortex. Here, we demonstrate that NMDA-induced injury forces endogenous Cell Tracker Green (CTG) labeled VZ/SVZ precursors out of the SVZ into the neurodegenerating cortex. CTG+/Nestin+/Filamin A+ precursors are closely associated with vimentin+/GFAP+/GLAST+ filaments and express both chemokine receptor CXCR4 and Robot. In the cortex, SVZ-derived progenitors show a progressive expression of developing, migrating and mature neurons and glial markers. CTG+/GFAP+ astrocytes greatly outnumber CTG+/MAP2+/NeuN+ neurons. SVZ-derived progenitors differentiate into both tbr1+ cortical glutamatergic neurons and calretinin+ interneurons. But, there is little integration of these neurons into the existing circuitry, as seen by Fluorogold retrograde tracing from the internal capsule. (C) 2008 Elsevier Inc. All rights reserved.

引用

页码：170 / 182

页数：13

共 54 条

[1] Primary cortical glial reaction versus secondary thalamic glial response in the excitotoxically injured young brain:: Microglial/macrophage response and major histocompatibility complex class I and II expression [J].