| Research BackgroundMechanical compression and secondary mechanisms may cause neurological deficit by influencing subtle structures of the cord. In the past, most investigators have considered that the axonal swellings in CMS trauma cases will degenerate. Furthermore, it has been thought that most axons in the CNS of mature mammals will fail to regenerate after trauma. However, recent studies have indicated that injured axons of the spinal cord and brain in fact may show some regenerative responses following injury by a way of growthconelike axonal terminals and aberrant axonal branching. Therefore, the idea is now proposed that axons of the CNS have an intrinsic potential for regeneration. A lot of efforts have been done to explore why axons of CNS cannot repair themselves as efficiently as those of the PNS and to find means by which CNS repair can be improved.Growth associated protein 43 (GAP-43) is a membrane-associated calmodulin-binding phosphoprotein present in the nervous system. It has been demonstrated that the protein is present in large quantities in the axonal growth cone, in outgrowing neurons in fetal and neonatal rat brain and spinal cord, and outgrowing processes of nerve growth factor differentiated PC 12 cells.Furthermore, the protein and its mRNA are re-expressed in regenerating axons following mechanical damage. Moreover, in the mature brain, GAP-43 expression declines sharply, but remains present in higher integrative areas of the brain such as the associative neocortex and the hippocampus. Taken together, these observations indicate that GAP-43 is associated with axonal out-growth and plasticity in the central nervous system (CNS).Microtubules have important structural and functional roles in neurons, particularly during development. They contribute to the generation and maintenance of the shape of nurites (undifferentiated axons and dendrites) and they provide structural support for fast axoplasmic transport. MAPI b is involved in microtubule assembly, cytoskeletal organization an organelle transport, and has recently been implicated in neurite outgrowth. The increased expression of MAP1B is thus considered as a marker for neurite regrowth in CNS.The neural cell adhesion molecule (NCAM), a cell surface glycoprotein, act as an homophilic ligand to promote cell to cell adhsion and thus take part I the regulation of cell-cell and cell-substrate inteactions. During axon outgrowth and axon extension in the developing nervous system, adhensive interactions between axon and glial cells o r between neurons have been shown to be mediated by NCAM. NCAM is highly concentrated in developing neural tissues, and in vitro studies show that it is localized in axonal growth cones and filopodia. In addition, NCAM mediated adhesive interactions have been shown to be important in very selective mechanisms such as target innervation and subsequent synapse formation. In some regions of the adult central nervous system, the embryonic form of NCAM could be detected, which might indicate the plasticity in these regions.It is well established that cholinergic neurons make up a significant proportion of the total neuronal pool in the spinal cord. The extent of spinal cord injury will thus be reflected by a reduction in the activity of choline acetyltransferase (ChAT), the enzyme that synthesizes acetylcholine. Theinjury-induced disappearance of ChAT only reflects a loss of such enzymes rather than actual neuronal death, and the rebound of ChAT activity after CNS injury is temporally associated with the partial recovery of function. Choline acetyitransferase can therefore be used as definitive marker for neuronal function in spinal cord injury.In contrast to experimental transection models, spinal cord compression demonstrates different neurophysiologic and neuropathologic features. Clinically, decompressive surgery is considered routine therapy for spinal cord compression. Accordingly, two types of spinal cord compression were analyzed: continuously compressed spinal cord, which could repre...
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