| Abstract: | We have shown previously that rubral axons grow around a lesion of their pathway in developing opossums and that a critical period exists for that plasticity. The critical period begins when rubral axons first reach the level of the lesion and ends sometime between postnatal days (PD) 26 and 30. The aim of the present study was to examine the development of an astrocytic response to lesioning the spinal cord to determine if there is a temporal correlation between the development of such a response and the end of the critical period. The astrocytic response was examined immunohistochemically, 2 and 4 weeks after hemisecting the thoracic spinal cord, using an antibody to glial fibrillary acidic protein (GFAP). A response was first seen at PD21 in the 2-week series. The response was relatively mild, however, and limited to the white matter. When the lesion was made at PD26. the response was still restricted to the white matter, but hypertrophied astrocytes were found at the gray/white matter junction and cystic cavities were present. When the lesion was made at PD41, the response had spread to the gray matter and it occupied a larger area rostral and caudal to the lesion than at earlier ages. The animals allowed to survive 4 weeks after lesioning were subjected to a second operation 4-5 days before sacrifice so that Fast Blue could be injected bilaterally two to three segments caudal to the lesion. When the hemisection was made at PD15, a response was present in the ventral and ventrolateral funiculi, but not in that part of the lateral funiculus that contains rubrospinal axons. As expected from previous studies, rubral neurons were labeled contralateral to the lesion, suggesting that their axons had grown around it. When the lesion was made at PD21, the glial response was still limited to the white matter, but it extended into that part of the lateral funiculus that contains rubral axons. In spite of the presence of a glial response, rubral neurons were still labeled contralateral to the lesion. When the lesion was made at PD26, hypertrophied astrocytes were present at the gray/white matter junction and small cavities were noted at the lesion site. In such cases, there was no evidence for rubrospinal plasticity. An astrocytic response was not observed in the gray matter of the dorsal horn, an area used by rubral axons to grow around a lesion of their pathway, until well after the end of the critical period. We conclude that the initial development of a glial scar in the white matter after lesioning does not determine the end of the critical period for rubrospinal plasticity. Loss of rubrospinal plasticity correlates most closely with the appearance of hypertrophied astrocytes at the gray/white matter junction and the formation of cystic cavities. |
