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Devastating motor, sensory, and autonomic dysfunctions render long-term personal hardships to the survivors of traumatic spinal cord injury (SCI). The suffering also extends to the survivors' families and friends, who endure emotional, physical, and financial burdens in providing for necessary surgeries, care, and rehabilitation. After the primary(More)
Upregulation of extracellular chondroitin sulfate proteoglycans (CSPGs) after CNS injuries contributes to the impediment of functional recovery by restricting both axonal regeneration and synaptic plasticity. In the present study, the effect of degrading CSPGs with the application of the bacterial enzyme chondroitinase ABC (chABC) into the cuneate nucleus(More)
After spinal cord injury (SCI), the absence of an adequate blood supply to injured tissues has been hypothesized to contribute to the lack of regeneration. In this study, blood vessel changes were examined in 28 adult female Fischer 344 rats at 1, 3, 7, 14, 28, and 60 days after a 12.5 g x cm NYU impactor injury at the T9 vertebral level. Laminin, collagen(More)
Identification of long tracts responsible for the initiation of spontaneous locomotion is critical for spinal cord injury (SCI) repair strategies. Pathways derived from the mesencephalic locomotor region and pontomedullary medial reticular formation responsible for fictive locomotion in decerebrate preparations project to the thoracolumbar levels of the(More)
Phospholipases A(2) (PLA(2)) are group of enzymes that hydrolyze membrane phospholipids at the sn-2 position. PLA(2) are present in the brain and spinal cord and are implicated in several neurological disorders. Previously, we showed that PLA(2) activity increases following traumatic spinal cord injury and injection of group III secretory PLA(2)(More)
Varying degrees of neurologic function spontaneously recovers in humans and animals during the days and months after spinal cord injury (SCI). For example, abolished upper limb somatosensory potentials (SSEPs) and cutaneous sensations can recover in persons post-contusive cervical SCI. To maximize recovery and the development/evaluation of repair(More)
Traumatic human spinal cord injury (SCI) causes devastating and long-term hardships. These are due to the irreparable primary mechanical injury and secondary injury cascade. In particular, oligodendrocyte cell death, white matter axon damage, spared axon demyelination, and the ensuing dysfunction in action potential conduction lead to the initial deficits(More)
Devastating central nervous system injuries and diseases continue to occur in spite of the tremendous efforts of various prevention programs. The enormity and annual escalation of healthcare costs due to them require that therapeutic strategies be responsibly developed. The dysfunctions that occur after injury and disease are primarily due to(More)
The aim of the present study was to characterize a novel electrophysiological assessment, the magnetically evoked interenlargement response (MIER), by defining the anatomical location of the fast conducting (large myelinated) ascending axons that mediate the response and the relationship between the response and locomotor function following experimental(More)
Increased chondroitin sulfate proteoglycan (CSPG) expression in the vicinity of a spinal cord injury (SCI) is a primary participant in axonal regeneration failure. However, the presence of similar increases of CSPG expression in denervated synaptic targets well away from the primary lesion and the subsequent impact on regenerating axons attempting to(More)