Degeneration of mammalian PNS and CNS axons is accelerated by incubation with protein synthesis inhibitors

Neurosci Res. 2003 Dec;47(4):445-9. doi: 10.1016/j.neures.2003.08.007.

Abstract

Protein synthesis inhibitors (PSIs) increase the rate of degeneration, as measured by compound action potential (CAP) conduction, in segments of rat PNS and CNS axons. Sciatic axonal segments maintained in vitro in Krebs at 37-38 degrees C generate CAPs for 24 h compared to 8 h for axons exposed to Krebs containing two PSIs, 100 microM anisomycin and/or 35 microM cycloheximide. Spinal axonal segments at 37-38 degrees C generate CAPs for 3 h compared to 2 h for axons exposed to Krebs containing PSIs. While cooling (6-9 degrees C) slows degeneration rate, cooled sciatic axons exposed to PSIs exhibit lower peak CAPs compared to cooled control segments (P<0.005).

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Action Potentials / drug effects
  • Animals
  • Anisomycin / pharmacology
  • Axons / drug effects*
  • Axons / pathology
  • Cold Temperature
  • Cycloheximide / pharmacology
  • Dose-Response Relationship, Drug
  • Female
  • Male
  • Organ Culture Techniques
  • Protein Synthesis Inhibitors / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Sciatic Nerve / drug effects
  • Sciatic Nerve / pathology
  • Spinal Cord / drug effects
  • Spinal Cord / pathology
  • Wallerian Degeneration / metabolism*

Substances

  • Protein Synthesis Inhibitors
  • Anisomycin
  • Cycloheximide