title: C6 deficiency does not alter intrinsic regeneration speed after peripheral nerve crush injury.
abstract: Peripheral nerve injury leads to Wallerian degeneration, followed by regeneration, in which functionality and morphology of the nerve are restored. We previously described that deficiency for complement component C6, which prevents formation of the membrane attack complex, slows down degeneration and results in an earlier recovery of sensory function after sciatic nerve injury compared to WT animals. In this study, we determine whether C6(-/-) rats have an intrinsic trait that affects sciatic nerve regeneration after injury. To study the contribution of complement activation on degeneration and regeneration with only minimal effect of complement activation, a crush injury model with only modest complement deposition was used. We compared the morphological and functional aspects of crushed nerves during degeneration and regeneration in C6(-/-) and WT animals. Morphological changes of myelin and axons showed similar degeneration and regeneration patterns in WT and C6(-/-) injured nerves. Functional degeneration and regeneration, recorded by ex vivo electrophysiology and in vivo foot flick test, showed that the timeline of the restoration of nerve conduction and sensory recovery also followed similar patterns in WT and C6(-/-) animals. Our findings suggest that C6 deficiency by itself does not alter the regrowth capacity of the peripheral nerve after crush injury.
authors.affiliation: Department of Genome analysis, UvA AMC, P.O. Box 22660, 1100 DD Amsterdam, The Netherlands. Electronic address: M.Sta@amc.nl.
authors.forename: M
authors.initials: M
authors.lastname: Sta
authors.affiliation: Cellular & Molecular Neurobiology, SILS - Center for Neuroscience, University of Amsterdam, P.O. Box 94215, 1090 GE Amsterdam, The Netherlands. Electronic address: N.Cappaert@uva.nl.
authors.forename: N L M
authors.initials: NL
authors.lastname: Cappaert
authors.affiliation: Department of Genome analysis, UvA AMC, P.O. Box 22660, 1100 DD Amsterdam, The Netherlands.
authors.forename: D
authors.initials: D
authors.lastname: Ramekers
authors.affiliation: Department of Genome analysis, UvA AMC, P.O. Box 22660, 1100 DD Amsterdam, The Netherlands. Electronic address: V.Ramaglia@amc.uva.nl.
authors.forename: V
authors.initials: V
authors.lastname: Ramaglia
authors.affiliation: Cellular & Molecular Neurobiology, SILS - Center for Neuroscience, University of Amsterdam, P.O. Box 94215, 1090 GE Amsterdam, The Netherlands. Electronic address: W.J.Wadman@uva.nl.
authors.forename: W J
authors.initials: WJ
authors.lastname: Wadman
authors.affiliation: Department of Genome analysis, UvA AMC, P.O. Box 22660, 1100 DD Amsterdam, The Netherlands. Electronic address: F.Baas@amc.nl.
authors.forename: F
authors.initials: F
authors.lastname: Baas
mesh_terms: D000818:Animals; D001369:Axons / Q000502:physiology; D003183:Complement C6 / Q000172:deficiency* / Q000502:physiology; D008297:Male; D009186:Myelin Sheath / Q000502:physiology; D009416:Nerve Regeneration; D059348:Peripheral Nerve Injuries / Q000503:physiopathology*; D051381:Rats; D012584:Sciatic Nerve / Q000293:injuries* / Q000502:physiology*; D014855:Wallerian Degeneration / Q000503:physiopathology
chemical_list: D003183:Complement C6
keywords: Complement system; Ex vivo electrophysiology; Morphology; Nerve crush; Peripheral nerve regeneration; Wallerian degeneration