Axonal transport of neurofilament proteins in IDPN neurotoxicity

J. W. Griffin, I. Parhad, B. Gold, D. L. Price, P. N. Hoffman, K. Fahnestock

Research output: Contribution to journalArticlepeer-review

Abstract

The neurofibrillary changes produced by IDPN are the consequence of the ability of the agent to impair the slow axonal transport of neurofilaments. The susceptibility of various neurons to this effect depends upon their neurofilament content; neurofilament-rich large caliber axons are severely affected. In motor neurons the half-velocities of neurofilament proteins are reduced 2-10 fold, while tubulin and other slow component constituents are only midly altered. Optic nerve fibers are intermediate in vulnerability and small neurofilamant-poor fibers have little change in slow transport. The agent acts directly on the axon, and the transport defect is expressed all along the course of susceptible axons. Similar alterations in neurofilament transort have recently been found with 3,4-dimethyl-2,5-hexanedione, indicating that similar pathogenetic mechanisms can occur with toxic agents other than IDPN.

Original languageEnglish (US)
Pages (from-to)43-54
Number of pages12
JournalNeuroToxicology
Volume6
Issue number4
StatePublished - 1985

ASJC Scopus subject areas

  • Neuroscience(all)
  • Toxicology

Fingerprint Dive into the research topics of 'Axonal transport of neurofilament proteins in IDPN neurotoxicity'. Together they form a unique fingerprint.

Cite this