This Article Full Text (PDF) References 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 Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Bittner, G. D. Articles by Peduzzi, J. D. Search for Related Content PubMed Articles by Bittner, G. D. Articles by Peduzzi, J. D. Social Bookmarking                         What's this?

Degeneration, Trophic Interactions, and Repair of Severed Axons: A Reconsideration of Some Common Assumptions

School of Biological Sciences (Neurobiology Section) and Institute of Neuroscience, The University of Texas at Austin, Austin, Texas

Timothy Schallert

School of Biological Sciences (Neurobiology Section) and Institute of Neuroscience, Department of Pyschology, The University of Texas at Austin, Austin, Texas

Jean D. Peduzzi

School of Optometry, Department of Physiological Optics, Injury Control and Vision Science Research Centers, University of Alabama at Birmingham, Birmingham, Alabama

We suggest that several interrelated properties of severed axons (degeneration, trophic dependencies, initial repair, and eventual repair) differ in important ways from commonly held assumptions about those properties. Specifically, (1) axotomy does not necessarily produce rapid degeneration of distal axonal segments because (2) the trophic maintenance of nerve axons does not necessarily depend entirely on proteins transported from the perikaryon—but instead axonal proteins can be trophically maintained by slowing their degradation and/or by acquiring new proteins via axonal synthesis or transfer from adjacent cells (e.g., glia). (3) The initial repair of severed distal or proximal segments occurs by barriers (seals) formed amid accumulations of vesicles and/or myelin delaminations induced by calcium influx at cut axonal ends—rather than by collapse and fusion of cut axolemmal leaflets. (4) The eventual repair of severed mammalian CNS axons does not necessarily have to occur by neuritic outgrowths, which slowly extend from cut proximal ends to possibly reestablish lost functions weeks to years after axotomy—but instead complete repair can be induced within minutes by polyethylene glycol to rejoin (fuse) the cut ends of surviving proximal and distal stumps. Strategies to repair CNS lesions based on fusion techniques combined with rehabilitative training and induced axonal outgrowth may soon provide therapies that can at least partially restore lost CNS functions.

Key Words: Axotomy • Axonal degeneration • Axonal regeneration • Axonal proteins • Spinal cord lesions • Recovery of function • Nerve plasticity

The Neuroscientist, Vol. 6, No. 2, 88-109 (2000)
DOI: 10.1177/107385840000600207


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?