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Complement activation after lumbosacral ventral root avulsion injury
Marcus Ohlsson1, Leif A Havton
1Department of Neurology and Brain Research Institute, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA 90095-1769, USA.
Neuroscience Letters
|November 18, 2005
Summary
Complement system activation contributes to motoneuron death after ventral root avulsion (VRA) injuries in adult rats. Inhibiting the membrane attack complex (MAC) may offer a neuroprotective strategy for cauda equina injuries.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Lumbosacral ventral root avulsion (VRA) causes motoneuron loss, partly via apoptosis.
- Caspase inhibitors fail to protect adult motoneurons post-VRA, suggesting alternative death mechanisms.
Purpose of the Study:
- Investigate the role of the complement system in adult rat motoneuron death following VRA.
- Determine if the membrane attack complex (MAC) contributes to neuronal injury.
Main Methods:
- Adult Sprague-Dawley rats underwent unilateral L5-S2 VRA.
- Quantitative immunohistochemistry assessed MAC and Clusterin expression at 10 days post-injury.
Main Results:
- The lytic MAC targeted approximately 38% of axotomized motoneurons.
- The MAC inhibitor Clusterin was upregulated in astrocytes and de novo in 30% of surviving motoneurons.
Conclusions:
- Complement activation and necrosis contribute to motoneuron death after VRA.
- Inhibiting MAC may be a potential neuroprotective strategy for cauda equina injuries.