EFFECTS OF FRONTAL CORTICAL-LESIONS ON MOUSE STRIATUM - REORGANIZATION OF CELL RECOGNITION MOLECULE, GLIAL FIBER, AND SYNAPTIC PROTEIN EXPRESSION IN THE DORSOMEDIAL STRIATUM

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 substa ntia nigra in animals with cerebral cortex lesions. Since cell recogni tion molecules are involved in the molecular mechanisms of contact bet ween cells and surrounding extracellular matrix components, and are im portant in plasticity of the nervous system, we investigated changes i n L1, N-CAM, and tenascin, as well as synapse-associated proteins and gliosis, in the striatum of mice with cortical lesions. The removal of somatosensory and motor cortex would be expected to produce changes p redominantly 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 t he striatum, as compared to the nonlesioned side. Tenascin expression was significantly decreased, but only in the most medial part of the s triatum. The changes in intensity of immunostaining with L1, N-CAM, an d tenascin did not diminish with time after lesioning. These changes i n cell recognition molecule expression indicate a possible molecular b asis of lesion-induced plasticity in neuronal circuits within the dors omedial striatum. These changes were accompanied by decreased synapsin and synaptophysin expression, but without any significant change in n eurofilament expression. In contrast, glial fibrillary acidic protein and vimentin immunoreactivities were increased in almost the entire st riatum on the lesioned side. Therefore, the areas of changes in cell r ecognition molecule expression did not simply correlate to the increas ed astrogliosis or neuronal fiber damage. We postulate that the perive ntricular dorsomedial striatum is relatively sensitive to disturbances of corticostriatonigral circuits and, simultaneously, this striatal a rea has a unique ability to support and promote neurite growth.