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This Article Full Text Full Text (PDF) All Versions of this Article: 95/6/3384    most recent 00350.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Shi, R. Articles by Whitebone, J. Search for Related Content PubMed PubMed Citation Articles by Shi, R. Articles by Whitebone, J.

Conduction Deficits and Membrane Disruption of Spinal Cord Axons as a Function of Magnitude and Rate of Strain

Department of Basic Medical Sciences, The Institute for Applied Neurology, School of Veterinary Medicine, and Weldon School of Biomedical Engineering, Purdue University, West Lafayette, Indiana

Submitted 4 April 2005; accepted in final form 21 February 2006

White matter strips extracted from adult guinea pig spinal cords were subjected to tensile strain (stretch) injury ex vivo. Strain was carried out at three magnitudes (25, 50, and 100%) and two strain rate regimens: slow (0.006–0.008 s^–1) and fast (355–519 s^–1). The cord samples were monitored physiologically using a double sucrose-gap technique and anatomically using a horseradish peroxidase assay. It seems that a higher magnitude of strain inflicted significantly more functional and structural damage within each strain rate group. Likewise, a higher strain rate inflicted more damage when the strain magnitude was maintained. It is evident that axons have remarkable tolerance to strain injury at a slow strain rate. Even a 100% strain at the slow rate only eliminated two-thirds of the compound action potential amplitude and resulted in almost no membrane damage when examined 30 min after strain. It is also clear that the spontaneous recovery is evident yet not complete compared with preinjury levels at the fast strain rate. To examine the factors that might influence the vulnerability of axons to strain, we have shown that the axonal diameters did not play a significant role in dictating the susceptibility of axons to strain. Rather, it is speculated that the location of axons might be a more important factor in this regard. The knowledge gained from this study is likely to be informative in elucidating the spinal cord biomechanical response to strain and strain rate.