Paraplegia, After Total Spinal Cord Transection in Mice

Abstract

Mice, in contrast to other species, have the ability to recover after severe spinal cord damage without any therapeutic intervention. We studied the development of Wallerian degeneration of the long spinal tracts and also the contribution of proliferative neuronal and glial cells after complete spinal cord transaction including the dura matter in C57bl/6 mice. In addition, we monitored the functional recovery in association with histological and immunohistochemical observations. Critical point of time after SCT was the second week, when the lesion reached its maximum size, was well-vascularized and begun to self-limit drastically, thereafter. However, slight degree of functional recovery began from 48 hours after spinal cord transection. Immunophenotype analysis of the proliferative cells revealed that endogenous neurogenesis was of the glial, and not of the neuronal cell-type proliferation. Glial cells seemed to almost completely replace cellular loss, to remyelinate spared axons, to restore blood barrier and to support the rest, undamaged, neurons. Intense proliferation of glial cells occurred in the first 48 hours after injury and began to decline thereafter. Consequently, therapeutic interventions aiming at stimulation of endogenous neurogenesis should be initiated within the first hours after injury, while new approaches should target at stimulating not only the glial but also the endogenous neuronal cell-type proliferation.