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This Article Full Text Full Text (PDF) All Versions of this Article: 90/4/2334    most recent 00868.2002v1 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 Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Jensen, J. M. Articles by Shi, R. Search for Related Content PubMed PubMed Citation Articles by Jensen, J. M. Articles by Shi, R.

Effects of 4-Aminopyridine on Stretched Mammalian Spinal Cord: The Role of Potassium Channels in Axonal Conduction

Department of Basic Medical Sciences, Center for Paralysis Research, Purdue University, West Lafayette, Indiana 47907

Submitted 30 September 2002; accepted in final form 6 July 2003

Axonal conduction deficit is a major contributor to various degrees of disability after spinal cord injury. 4-aminopyridine (4-AP), a potassium channel blocker, has been shown to restore some conduction and improve neurological function in both animal and human studies. Using a double sucrosegap recording device, we have examined the effects of 4-AP on isolated guinea pig spinal cord white matter after stretch injury. At a concentration of 100 µM, 4-AP increased the amplitude of the compound action potential by 100% while 1 µM 4-AP increased it by 43%, a larger response than seen following compression injury. The length of affected tissue is suggested as a potential explanation of this differential sensitivity to 4-AP. Plastic sections taken from the injury site revealed severe myelin damage, especially in the paranodal area, which may also partially explain why 4-AP has more effect on conduction after stretch injury than compression. In addition, we have shown that while enhancing conductivity in some axons, 4-AP significantly reduced the overall responsiveness to multiple stimuli, as evidenced by increase of the refractory period in response to dual stimuli and the decreased ability to follow repetitive stimuli. This increased refractoriness may be largely attributed to residual deficits in fibers newly recruited by 4-AP treatment.

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