QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, April 9, 2008, 28(15):3887-3896; doi:10.1523/JNEUROSCI.4756-07.2008

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Lasiene, J. Articles by Horner, P. PubMed PubMed Citation Articles by Lasiene, J. Articles by Horner, P.

 Previous Article  |  Next Article 

Development/Plasticity/Repair
No Evidence for Chronic Demyelination in Spared Axons after Spinal Cord Injury in a Mouse

Jurate Lasiene,^1,2 Larry Shupe,³ Steve Perlmutter,³ and Philip Horner¹

Departments of ¹Neurological Surgery, ²Psychology, and ³Physiology and Biophysics, University of Washington, Seattle, Washington 98195

Correspondence should be addressed to Philip Horner, Department of Neurological Surgery, University of Washington, Seattle, WA 98195. Email: phorner{at}u.washington.edu

The pattern of remyelination after traumatic spinal cord injury remains elusive, with animal and human studies reporting partial to complete demyelination followed by incomplete remyelination. In the present study, we found that spared rubrospinal tract (RST) axons of passage traced with actively transported dextrans and examined caudally to the lesion 12 weeks after mouse spinal cord contusion injury were fully remyelinated. Spared axons exhibited a marginally reduced myelin thickness and significantly shorter internodes. CASPR (contactin-associated protein) and K_v1.2 channels were used to identify internodes and paranodal protein distribution properties were used as an index of myelin integrity. This is the first time the CNS myelin internode length was measured in a mouse. To better understand the significance of shortened internodes and thinner myelin in spared axons, we modeled conduction properties using McIntyre's et al. model of myelinated axons. Mathematical modeling predicted a 21% decrease in the conduction velocity of remyelinated RST axons attributable to shortened internodes. To determine whether demyelination could be present on axons exhibiting a pathological transport system, we used the retroviral reporter system. Virally delivered green fluorescent protein unveiled a small population of dystrophic RST axons that persist chronically with evident demyelination or abnormal remyelination. Collectively, these data show that lasting demyelination in spared axons is rare and that remyelination of axons of passage occurs in the chronically injured mouse spinal cord.

Key words: myelin; remyelination; CASPR; trauma; mouse; conduction; internode; spinal cord injury; axons

---

Received Dec. 29, 2006; revised Feb. 25, 2008; accepted Feb. 25, 2008.

Correspondence should be addressed to Philip Horner, Department of Neurological Surgery, University of Washington, Seattle, WA 98195. Email: phorner{at}u.washington.edu

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help