Astrocytic development, astrocytic scar formation and myelin formation as possible factors in loss of rubrospinal plasticity

Rubral axons can grow around a lesion of their spinal pathway in developing opossums and a critical period exists for that plasticity (Martin and Xu, Dev. Brain Res., 39:303-308). Such plasticity results primarily from new growth but regeneration also occurs (Xu and Martin, J. Comp. Neurol., 313:103-112). The end of the critical period could result from lack of new growth, but it may also be related to factors in the environment. The aim of our studies was to determine if an astrocytic response to injury and/or myelin formation correlates temporally with the end of the critical period.; Before we addressed the issue of an astrocytic response we studied astrocytic development by using vimentin and glial fibrillary acidic protein (GFAP) immunohistochemistry. The development of GFAP-LI in radial glia and the transformation of radial glia into mature appearing astrocytes followed ventral to dorsal and rostral to caudal gradients. In the areas occupied by rubral axons as they grow around a lesion, this transformation occured at approximately the end of the critical period.; We studied the development of an astrocytic response to lesioning the rubrospinal tract at thoracic levels by using GFAP immunohistochemistry. We observed an astrocytic response in the white matter before the end of the critical period but it did not spread to the grey matter until well after plasticity was lost. The early response may not have influenced plasticity since rubral axons can use the grey matter to circumvent the lesion. By the end of the critical period, however, a few hypertrophied astrocytes were present in the grey/white matter junction and small cystic cavitations were present in the white matter. We conclude that the initial appearance of a glial response is not a major deterrant to late growing or regenerating axons.; We studied myelin formation by using myelin basic protein (MBP) and galactocerebroside (GalC) immunohistochemistry. MBP- and GalC-LI were not present in either the dorsal part of the lateral funiculus or the dorsal horn at thoracic levels, areas where myelin proteins could inhibit rubral axons, until a week after the end of the critical period. If rubral axons take a week to grow around a lesion, however, or if proteins which inhibit axonal growth appear before MBP or GalC-LI can be demonstrated, it is possible that the development of myelin helps determine the end of the critical period.