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基质金属蛋白酶-2参与耳蜗损伤后的突触重塑。

MMP-2 is involved in synaptic remodeling after cochlear lesion.

作者信息

Fredrich Michaela, Illing Robert-Benjamin

机构信息

Neurobiological Research Laboratory, Department of Otorhinolaryngology, University of Freiburg, Freiburg, Germany.

出版信息

Neuroreport. 2010 Mar 31;21(5):324-7. doi: 10.1097/WNR.0b013e328335b518.

DOI:10.1097/WNR.0b013e328335b518
PMID:20173666
Abstract

Lesion-induced neuroplasticity, including fiber degeneration, axonal growth, and synaptogenesis, involves dynamical changes of the extracellular matrix. We discovered that the matrix metalloprotease-2 (MMP-2), a major actor in extracellular matrix recomposition, is changed in distribution and increased in amount in the ventral cochlear nucleus after unilateral cochlear ablation. There was a remarkable coincidence of MMP-2 accumulation and GAP-43 expression in time and space. We obtained evidence indicating that MMP-2 is delivered to regions of emerging GAP-43 positive synaptic endings by postsynaptic neurons as well as by adjoining astrocytes. These results indicate a major role of MMP-2 in lesion-induced remodeling of central auditory networks and suggest a cooperativity with GAP-43-directed axonal outgrowth and synaptogenesis.

摘要

损伤诱导的神经可塑性,包括纤维变性、轴突生长和突触形成,涉及细胞外基质的动态变化。我们发现,基质金属蛋白酶-2(MMP-2)作为细胞外基质重组的主要参与者,在单侧耳蜗切除术后,其在蜗腹侧核中的分布发生变化且数量增加。MMP-2的积累与GAP-43的表达在时间和空间上存在显著的一致性。我们获得的证据表明,MMP-2由突触后神经元以及相邻的星形胶质细胞传递到出现GAP-43阳性突触末梢的区域。这些结果表明MMP-2在损伤诱导的中枢听觉网络重塑中起主要作用,并提示其与GAP-43导向的轴突生长和突触形成存在协同作用。

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