• C Laramore, E Maymind, and M I Shifman.
• Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
• Neuroscience. 2011 Jun 2; 183: 265-77.

AbstractExogenous neurotrophins reduce neuronal atrophy and promote regeneration following spinal cord injury but little is known about the endogenous expression of neurotrophins and their tropomyosin-related kinase (Trk) receptors in the injured spinal cord. For this purpose, we used the larval lamprey because it recovers from complete spinal transection and axons regenerate selectively in their correct paths. We cloned lamprey neurotrophin (NT) and its two Trk receptors and assessed their mRNA expression by in situ hybridization and QRT-PCR in control animals and after spinal cord transection. Control lampreys showed a longitudinal array of NT-expressing neurons along length of the spinal cord. At 2 weeks post-transection, NT expression was downregulated in neurons close to the transection, but was little affected remote from the lesion. By 4 weeks, NT expression returned to control levels in spinal cord neurons rostral and caudal to the lesion, although it was upregulated in reactive microglia at 14 and 30 days post-transection. Double-label in situ hybridization for Trk1 and Trk2 showed that Trk transcripts were expressed in several giant reticulospinal neurons, including the Mauthner neurons. After spinal cord transection, Trk1 mRNA expression was downregulated, but Trk2 mRNA expression was not changed or was increased. Thus, our data suggest that spinal cord injury in larval lampreys modulate expression of endogenous neurotrophin and induces proliferation of macrophage/microglial cells that express neurotrophin.Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.

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