Department of Cell Morphology & Molecular Neurobiology, Ruhr-University, Universitätsstraße 150, 44801 Bochum, Germany.
Cell Tissue Res. 2012 Jul;349(1):133-45. doi: 10.1007/s00441-011-1313-4. Epub 2012 Jan 26.
CNS lesions generally result in impaired function because regeneration of the adult CNS of mammals is poor. A variety of lesion models has been described that serve to further the understanding of the pathophysiology of the damaged tissue. A central cause of aborted regeneration is the glial scar that expresses a plethora of extracellular matrix molecules. Some of these are considered inhibitors of axon growth and regeneration. The laser lesion of the cortex offers the advantage that a circumscribed lesion of defined energy can be delivered to the cortex non-invasively through the intact dura mater and a thinly drilled wet translucent remnant of the skull. Previously, we have shown that distinct ECM is up-regulated in the penumbra of laser lesions in the rat visual cortex. We propose to transfer this model to the mouse, in view of the availability of a large number of genetical models in this small rodent. Here, we discuss this model and the lesion-related ECM that forms the focus of our analysis.
中枢神经系统损伤通常会导致功能障碍,因为哺乳动物的成年中枢神经系统再生能力很差。已经描述了多种损伤模型,这些模型有助于进一步了解损伤组织的病理生理学。导致再生失败的一个主要原因是星形胶质细胞瘢痕,它表达大量细胞外基质分子。其中一些被认为是轴突生长和再生的抑制剂。皮质激光损伤的优点是可以通过完整的硬脑膜和颅骨上薄薄钻过的湿半透明残余物,将限定能量的局灶性损伤非侵入性地递送到皮质。以前,我们已经表明,在大鼠视觉皮质的激光损伤的半影区中,特定的细胞外基质会被上调。鉴于这种小型啮齿动物中有大量的遗传模型,我们拟将该模型转移到小鼠中。在这里,我们讨论了该模型和形成我们分析重点的与损伤相关的细胞外基质。