Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 210, Issue 1-2, Pages 52-62Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2009.01.028
Keywords
Complement; Neurofilament; C5aR; Glutamate; Amyotrophic lateral sclerosis; Excitotoxicity
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Funding
- Muscular Dystrophy Association (Tucson)
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In NFL-/- mice, a model of motor neuron degeneration in ALS, degenerating spinal motor neurons express high levels of the receptor for the C5a anaphylatoxin (C5aR) early in the disease process. C-5a is a potent in vitro neurotoxin for both Neuro2A and NGF-differentiated PC12 cells. While no interaction was observed between glutamate and C5a, both C5a and kainate upregulated the expression of activated C5aR. C5aR expression was increased in motor neurons in ALS. This data suggests that the early upregulation of C5aR may contribute to motor neuron damage that potentiates excitotoxicity in ALS. (C) 2009 Elsevier B.V. All rights reserved.
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