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β,β′‐Iminodipropionitrile Impairs Retrograde Axonal Transport
Author(s) -
Fink David J.,
Purkiss David,
Mata Marina
Publication year - 1986
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1986.tb00717.x
Subject(s) - axoplasmic transport , neurofilament , neurotoxin , neurotoxicity , sciatic nerve , cell bodies , axotomy , chemistry , intraperitoneal injection , anatomy , toxicity , central nervous system , neuroscience , medicine , biology , endocrinology , biochemistry , immunohistochemistry
β,β′‐Iminodipropionitrile (IDPN), a neurotoxin, causes redistribution of neurofilaments in axons followed by the development of proximal axonal swellings and, in chronic intoxication, a distal decrease in axonal caliber. The latter changes are caused by a selective impairment in the slow anterograde axonal transport of neurofilament proteins. To assess the role of retrograde axonal transport in IDPN toxicity, we used [ 3 H] N ‐succinimidyl propionate ([ 3 H]NSP) to label covalently endogenous axonal proteins in sciatic nerve of the rat and measured the accumulation of radioactively labeled proteins in the cell bodies of motor and sensory neurons over time. IDPN was injected intraneurally 6 h or intraperitoneally 1 day before subepineurial injection of [ 3 H]NSP into the sciatic nerve, and the animals were killed 1, 2, and 7 days after [ 3 H]NSP injection. Neurotoxicity was assessed by electron microscopic observation of the nerves of similarly treated animals. Both intraneural and intraperitoneal injection of IDPN caused an acute reduction in the amount of labeled proteins transported back to the cell bodies. The early appearance of these changes suggests that alterations in retrograde transport may play a role in the production of the neuropathic changes.