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Genetic approaches to autonomic dysreflexia.
1Biotherapeutics Research Group, The Spinal Cord Injury Team, Robarts Research Institute and The Graduate Program in Neuroscience, The University of Western Ontario, P.O. Box 5015, 100 Perth Drive, London, ON N6A 5K8, Canada. abrown@robarts.ca
Progress in Brain Research
|October 4, 2005
Summary
Autonomic dysreflexia incidence is reduced in Wallerian degeneration slow (Wld s) mice after spinal cord injury. Axonal degeneration may trigger this life-threatening condition, suggesting new research avenues.
Area of Science:
- Neuroscience
- Genetics
- Physiology
Background:
- Autonomic dysreflexia (AD) is a dangerous complication following spinal cord injury (SCI) above the mid-thoracic level.
- The molecular mechanisms driving AD development remain poorly understood.
- Mice offer a valuable model for studying AD due to their sequenced genome and genetic resources.
Purpose of the Study:
- To investigate the role of axonal degeneration in the development of autonomic dysreflexia.
- To compare AD incidence and severity in different mouse strains and injury models.
Main Methods:
- Spinal cord transection and clip-compression injuries were performed on wild-type mice (129Sv and C57BL/6) and a spontaneous mutant (Wallerian degeneration slow, Wld s).
- Autonomic dysreflexia incidence and amplitude were measured and compared between groups.
Main Results:
- Wld s mice exhibited significantly reduced AD incidence compared to wild-type mice after both injury types.
- Clip-compression injury in 129Sv and C57BL/6 mice also led to reduced AD incidence.
- The amplitude of the dysreflexic response was greater in 129Sv than in C57BL/6 mice following clip-compression injury.
Conclusions:
- Axonal degeneration is implicated as a significant trigger for autonomic dysreflexia.
- Mouse genetics and interstrain differences play a role in AD development.
- These findings provide insights into potential molecular mechanisms underlying AD post-SCI.