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The Journal of Neuroscience, December 17, 2008, 28(51):13876-13888; doi:10.1523/JNEUROSCI.2823-08.2008

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Development/Plasticity/Repair
Deficiency in Complement C1q Improves Histological and Functional Locomotor Outcome after Spinal Cord Injury

Manuel D. Galvan,^1,2 Sabina Luchetti,^1,2 Adrian M. Burgos,^1,2 Hal X. Nguyen,^1,2 Mitra J. Hooshmand,^1,2 Frank P. T. Hamers,³ and Aileen J. Anderson^1,2

Departments of ¹Physical Medicine & Rehabilitation and ²Anatomy & Neurobiology, Reeve-Irvine Research Center, University of California, Irvine, Irvine, California 92697-4292, and ³Rehabilitation Hospital "DE Hoogstraat," Rudolf Magnus Institute of Neuroscience, 3583 TM Utrecht, The Netherlands

Correspondence should be addressed to Aileen J. Anderson, Departments of Physical Medicine & Rehabilitation and Anatomy & Neurobiology, University of California, Irvine, 1107 Gillespie Neuroscience Research Facility, Irvine, CA 92697-4540. Email: aja{at}uci.edu

Although studies have suggested a role for the complement system in the pathophysiology of spinal cord injury (SCI), that role remains poorly defined. Additionally, the relative contribution of individual complement pathways in SCI is unknown. Our initial studies revealed that systemic complement activation was strongly influenced by genetic background and gender. Thus, to investigate the role of the classical complement pathway in contusion-induced SCI, male C1q knock-out (KO) and wild-type (WT) mice on a complement sufficient background (BUB) received a mild-moderate T9 contusion injury with the Infinite Horizon impactor. BUB C1q KO mice exhibited greater locomotor recovery compared with BUB WT mice (p < 0.05). Improved recovery observed in BUB C1q KO mice was also associated with decreased threshold for withdrawal from a mild stimulus using von Frey filament testing. Surprisingly, quantification of microglia/macrophages (F4/80) by FACS analysis showed that BUB C1q KO mice exhibited a significantly greater percentage of macrophages in the spinal cord compared with BUB WT mice 3 d post-injury (p < 0.05). However, this increased macrophage response appeared to be transient as stereological assessment of spinal cord tissue obtained 28 d post-injury revealed no difference in F4/80-positive cells between groups. Stereological assessment of spinal cord tissue showed that BUB C1q KO mice had reduced lesion volume and an increase in tissue sparing compared with BUB WT mice (p < 0.05). Together, these data suggest that initiation of the classical complement pathway via C1q is detrimental to recovery after SCI.

Key words: complement system; C1q; spinal cord injury; inflammation; transgenic mice; locomotor function

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Received June 19, 2008; revised Sept. 29, 2008; accepted Oct. 24, 2008.

Correspondence should be addressed to Aileen J. Anderson, Departments of Physical Medicine & Rehabilitation and Anatomy & Neurobiology, University of California, Irvine, 1107 Gillespie Neuroscience Research Facility, Irvine, CA 92697-4540. Email: aja{at}uci.edu

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