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The Journal of Neuroscience, July 2, 2008, 28(27):6836-6847; doi:10.1523/JNEUROSCI.5372-07.2008

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Cellular/Molecular
Regenerative Growth of Corticospinal Tract Axons via the Ventral Column after Spinal Cord Injury in Mice

Oswald Steward,^1,2 Binhai Zheng,³ Marc Tessier-Lavigne,⁴ Maura Hofstadter,¹ Kelli Sharp,¹ and Kelly Matsudaira Yee¹

¹Reeve-Irvine Research Center and ²Departments of Anatomy and Neurobiology, and Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697-4292, ³Department of Neurosciences, University of California at San Diego, La Jolla, California 92093, and ⁴Genentech, Inc., South San Francisco, California 94080

Correspondence should be addressed to Dr. Oswald Steward, Reeve-Irvine Research Center, University of California, Irvine, 1105 Gillespie Neuroscience Research Facility, Irvine, CA 92697-4292. Email: osteward{at}uci.edu

Studies that have assessed regeneration of corticospinal tract (CST) axons in mice after genetic modifications or other treatments have tacitly assumed that there is little if any regeneration of CST axons in normal mice in the absence of some intervention. Here, we document a previously unrecognized capability for regenerative growth of CST axons in normal mice that involves growth past the lesion via the ventral column. Mice received dorsal hemisection injuries at thoracic level 6–7, which completely transect descending CST axons in the dorsal and dorsolateral column. Corticospinal projections were traced by injecting biotinylated dextran amine (BDA) into the sensorimotor cortex of one hemisphere either at the time of the injury or 4 weeks after injury, and mice were killed at 20–23 or 46 d after injury. At 20–23 d after injury, BDA-labeled CST axons did not extend past the lesion except in one animal. By 46 d after injury, however, a novel population of BDA-labeled CST axons could be seen extending from the gray matter rostral to the injury into the ventral column, past the lesion, and then back into the gray matter caudal to the injury in which they formed elaborate terminal arbors. The number of axons with this highly unusual trajectory was small (1% of the total number of labeled CST axons rostral to the injury). The BDA-labeled axons in the ventral column were on the same side as the main tract and thus are not spared ventral CST axons (which would be contralateral to the main tract). These results indicate that normal mice have a capacity for CST regeneration that has not been appreciated previously, which has important implications in studying the effect of genetic or pharmacological manipulations on CST regeneration in mice.

Key words: spinal cord injury; corticospinal tract; axon regeneration; sprouting; motor system; mice; biotinylated dextran amine; BDA; tract tracing

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Received Dec. 4, 2007; revised May 20, 2008; accepted May 21, 2008.

Correspondence should be addressed to Dr. Oswald Steward, Reeve-Irvine Research Center, University of California, Irvine, 1105 Gillespie Neuroscience Research Facility, Irvine, CA 92697-4292. Email: osteward{at}uci.edu

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