Abstract

The sequence of changes in transected rat sciatic nerves were subjected to parallel ultrastructural and biochemical studies. Widespread granular disintegration of axoplasmic microtubules and neurofilaments occurred in the 24--72 hour interval following nerve transection. These changes were associated with a loss of neurofilament proteins and a marked enhancement of 53,000, 70--73,000 and 85,000 MW proteins in transected nerve. The emergence of prominent nerve proteins during the aftermath of axonal degeneration supports their derivation from axonal sources. These three proteins remained prominent components in transected nerves and comprised the major proteins found in 34-day transected nerves. Amorphous granular breakdown products from myelinated and unmyelinated nerve fibers were encountered with progressively decreasing frequency after 48 hours. This diminution of intracellular axonal debris was accompanied by the appearance and increasing prominence of amorphous granular deposits within the endoneurium of transected nerves. These endoneurial deposits became closely associated with collagen fibers and persisted as a prominent component in 34-, 80- and 120-day transected nerves. It is suggested that the amorphous endoneurial granular deposits arise in part from the externalization of granular axoplasmic breakdown products. Externalized axonal components could have important implications for tissue reaction to injury.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.