Schüppel Karin, Brauer Kurt, Härtig Wolfgang, Grosche Jens, Earley Bernadette, Leonard Brian E, Brückner Gert
Department of Neurochemistry, Paul Flechsig Institute for Brain Research, University of Leipzig, Jahnallee 59, D-04109 Leipzig, Germany.
Brain Res. 2002 Dec 27;958(2):448-53. doi: 10.1016/s0006-8993(02)03569-2.
The destruction of the extracellular matrix by inflammatory processes may induce neuronal dysfunction and accelerate neurodegeneration. We describe that chondroitin sulphate proteoglycan-immunoreactive perineuronal nets and the enwrapped interneurons persisted 2 weeks after trimethyltin intoxication of rats (TMT, 8 mg/kg, i.p.) in all regions of the severely affected hippocampus and dentate gyrus, whereas the diffuse immunoreactivity around the CA2 pyramidal cells was reduced. Fluoro-Jade staining of degenerating neurons and staining of microglia by Griffonia simplicifolia agglutinin showed that net-associated neurons survived in the vicinity of damaged pyramidal cells and that perineuronal nets were not removed by activated microglia. We conclude that the extracellular matrix of perineuronal nets resists destruction after TMT treatment in the inflamed neural tissue. A permanent reconstitution of matrix components may be one of the factors that may support the viability of distinct types of neurons during neurodegenerative diseases.
炎症过程对细胞外基质的破坏可能会诱发神经元功能障碍并加速神经退行性变。我们发现，在大鼠经三甲基锡（TMT，8 mg/kg，腹腔注射）中毒后2周，硫酸软骨素蛋白聚糖免疫反应性的神经元周围网以及被包裹的中间神经元在严重受损的海马体和齿状回的所有区域均持续存在，而CA2锥体细胞周围的弥漫性免疫反应性则降低。对退化神经元的氟玉染色以及用西非吊灯树凝集素对小胶质细胞进行染色显示，与网相关的神经元在受损锥体细胞附近存活，并且神经元周围网未被活化的小胶质细胞清除。我们得出结论，在炎症神经组织中，TMT处理后神经元周围网的细胞外基质能够抵抗破坏。基质成分的永久性重建可能是在神经退行性疾病期间支持不同类型神经元存活的因素之一。
