• J E Jacob, P Gris, M G Fehlings, L C Weaver, and A Brown.
• BioTherapeutics Research Group, The Robarts Research Institute and The Graduate Program in Neuroscience, The University of Western Ontario, 100 Perth Drive, London, Ontario, Canada N6A 5K8.
• Exp. Neurol. 2003 Sep 1; 183 (1): 136-46.

AbstractTo study plasticity of central autonomic circuits that develops after spinal cord injury (SCI), we have characterized a mouse model of autonomic dysreflexia. Autonomic dysreflexia is a condition in which episodic hypertension occurs after injuries above the midthoracic segments of the spinal cord. As synaptic plasticity may be triggered by axonal degeneration, we investigated whether autonomic dysreflexia is reduced in mice when axonal degeneration is delayed after SCI. We subjected three strains of mice, Wld(S), C57BL, and 129Sv, to either spinal cord transection (SCT) or severe clip-compression injury (CCI). The Wld(S) mouse is a well-characterized mutant that exhibits delayed Wallerian degeneration. The CCI model is an injury paradigm in which significant the axonal degeneration is due to secondary events and therefore delayed relative to the time of the initial injury. We herein demonstrate that the incidence of autonomic dysreflexia is reduced in Wld(S) mice after SCT and in all mice after CCI. To determine if differences in afferent arbor sprouting could explain our observations, we assessed changes in the afferent arbor in each mouse strain after both SCT and CCI. We show that independent of the type of injury, 129Sv mice but not C57BL or Wld(S) mice demonstrated an increased small-diameter CGRP-immunoreactive afferent arbor after SCI. Our work thus suggests a role for Wallerian degeneration in the development of autonomic dysreflexia and demonstrates that the choice of mouse strain and injury model has important consequences to the generalizations that may be drawn from studies of SCI in mice.

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