Poltorak M, Herranz A S, Williams J, Lauretti L, Freed W J
Preclinical Neurosciences Section, Neuropsychiatry Branch, NIMH Neuroscience Center, St. Elizabeth's, Washington, DC 20032.
J Neurosci. 1993 May;13(5):2217-29. doi: 10.1523/JNEUROSCI.13-05-02217.1993.
Brain injury induces trophic effects within adjacent tissue through an unknown molecular mechanism. One model of this lesion effect involves the enhanced outgrowth of neuronal processes from transplanted substantia nigra in animals with cerebral cortex lesions. Since cell recognition molecules are involved in the molecular mechanisms of contact between cells and surrounding extracellular matrix components, and are important in plasticity of the nervous system, we investigated changes in L1, N-CAM, and tenascin, as well as synapse-associated proteins and gliosis, in the striatum of mice with cortical lesions. The removal of somato-sensory and motor cortex would be expected to produce changes predominantly in the dorsal striatum. Lesioned mice, however, showed a significant enhancement of both L1 and N-CAM immunostaining intensity only within the most medial-periventricular and dorsomedial parts of the striatum, as compared to the nonlesioned side. Tenascin expression was significantly decreased, but only in the most medial part of the striatum. The changes in intensity of immunostaining with L1, N-CAM, and tenascin did not diminish with time after lesioning. These changes in cell recognition molecule expression indicate a possible molecular basis of lesion-induced plasticity in neuronal circuits within the dorsomedial striatum. These changes were accompanied by decreased synapsin and synaptophysin expression, but without any significant change in neurofilament expression. In contrast, glial fibrillary acidic protein and vimentin immunoreactivities were increased in almost the entire striatum on the lesioned side. Therefore, the areas of changes in cell recognition molecule expression did not simply correlate to the increased astrogliosis or neuronal fiber damage. We postulate that the periventricular dorsomedial striatum is relatively sensitive to disturbances of corticostriatonigral circuits and, simultaneously, this striatal area has a unique ability to support and promote neurite growth.
脑损伤通过未知的分子机制在相邻组织内诱导营养作用。这种损伤效应的一种模型涉及在患有大脑皮层损伤的动物中，移植的黑质神经元突起的生长增强。由于细胞识别分子参与细胞与周围细胞外基质成分之间接触的分子机制，并且在神经系统的可塑性中起重要作用，我们研究了L1、N-CAM和腱生蛋白以及突触相关蛋白和胶质增生在患有皮层损伤的小鼠纹状体中的变化。躯体感觉和运动皮层的切除预计主要会在背侧纹状体中产生变化。然而，与未损伤侧相比，损伤小鼠仅在纹状体最内侧脑室周围和背内侧部分内显示L1和N-CAM免疫染色强度显著增强。腱生蛋白表达显著降低，但仅在纹状体最内侧部分。损伤后，L1、N-CAM和腱生蛋白免疫染色强度的变化并未随时间减弱。这些细胞识别分子表达的变化表明背内侧纹状体内神经元回路损伤诱导可塑性的可能分子基础。这些变化伴随着突触素和突触囊泡蛋白表达的降低，但神经丝表达没有任何显著变化。相反，损伤侧几乎整个纹状体内胶质纤维酸性蛋白和波形蛋白免疫反应性增加。因此，细胞识别分子表达变化的区域与星形胶质细胞增生增加或神经元纤维损伤并不简单相关。我们推测脑室周围背内侧纹状体对皮质纹状体黑质回路的干扰相对敏感，同时，这个纹状体区域具有支持和促进神经突生长的独特能力。
