Clioquinol and 2,5-hexanedione induce different types of distal axonopathy in the dog

G. Krinke, H. H. Schaumburg, Peter Spencer, P. Thomann, R. Hess

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

The central distal axonopathy induced in dogs by the administration of high doses of clioquinol is contrasted with the central-peripheral distal axonopathy precipitated by intoxication with 2,5-hexanedione. Mature, pure-bred Beagle dogs received a daily oral dose of 400 mg/kg of clioquinol for up to 7 months, or 1 ml per animal (approximately corresponding to 110 mg/kg) of 2,5-hexanedione for up to 5 months. Intoxicated and control animals were killed and perfused at monthly intervals, so that the spatial-temporal development of the lesion could be followed and correlated with clinical symptoms. During the treatment, dogs intoxicated with 2,5-hexanedione developed symptoms of peripheral neuropathy consisting of flaccid weakness, muscle atrophy, hind-limb foot-drop and areflexia. By contrast, the dogs surviving clioquinol intoxication exhibited a stiff-legged gait, hyperreflexia but no muscle atrophy. Light and electron microscope examination of central and peripheral nervous tissue from dogs intoxicated with 2,5-hexanedione revealed giant axonal swelling and distal axonal degeneration. By contrast, dogs receiving clioquinol showed a distal axonal degeneration confined to the optic tract and the long spinal cord tracts, without any visible involvement of peripheral nerves.

Original languageEnglish (US)
Pages (from-to)213-221
Number of pages9
JournalActa Neuropathologica
Volume47
Issue number3
DOIs
StatePublished - Jan 1979
Externally publishedYes

Fingerprint

Clioquinol
Dogs
Muscular Atrophy
Nerve Tissue
Abnormal Reflexes
Peripheral Nervous System Diseases
Gait
Peripheral Nerves
2,5-hexanedione
Foot
Spinal Cord
Extremities
Electrons
Light

Keywords

  • 2,5-hexanedione
  • Clioquinol
  • Distal axonopathy
  • Dog
  • Intoxication

ASJC Scopus subject areas

  • Neuroscience(all)
  • Pathology and Forensic Medicine
  • Clinical Neurology

Cite this

Clioquinol and 2,5-hexanedione induce different types of distal axonopathy in the dog. / Krinke, G.; Schaumburg, H. H.; Spencer, Peter; Thomann, P.; Hess, R.

In: Acta Neuropathologica, Vol. 47, No. 3, 01.1979, p. 213-221.

Research output: Contribution to journalArticle

Krinke, G. ; Schaumburg, H. H. ; Spencer, Peter ; Thomann, P. ; Hess, R. / Clioquinol and 2,5-hexanedione induce different types of distal axonopathy in the dog. In: Acta Neuropathologica. 1979 ; Vol. 47, No. 3. pp. 213-221.
@article{df07b2750419468a9e1bcb956191c107,
title = "Clioquinol and 2,5-hexanedione induce different types of distal axonopathy in the dog",
abstract = "The central distal axonopathy induced in dogs by the administration of high doses of clioquinol is contrasted with the central-peripheral distal axonopathy precipitated by intoxication with 2,5-hexanedione. Mature, pure-bred Beagle dogs received a daily oral dose of 400 mg/kg of clioquinol for up to 7 months, or 1 ml per animal (approximately corresponding to 110 mg/kg) of 2,5-hexanedione for up to 5 months. Intoxicated and control animals were killed and perfused at monthly intervals, so that the spatial-temporal development of the lesion could be followed and correlated with clinical symptoms. During the treatment, dogs intoxicated with 2,5-hexanedione developed symptoms of peripheral neuropathy consisting of flaccid weakness, muscle atrophy, hind-limb foot-drop and areflexia. By contrast, the dogs surviving clioquinol intoxication exhibited a stiff-legged gait, hyperreflexia but no muscle atrophy. Light and electron microscope examination of central and peripheral nervous tissue from dogs intoxicated with 2,5-hexanedione revealed giant axonal swelling and distal axonal degeneration. By contrast, dogs receiving clioquinol showed a distal axonal degeneration confined to the optic tract and the long spinal cord tracts, without any visible involvement of peripheral nerves.",
keywords = "2,5-hexanedione, Clioquinol, Distal axonopathy, Dog, Intoxication",
author = "G. Krinke and Schaumburg, {H. H.} and Peter Spencer and P. Thomann and R. Hess",
year = "1979",
month = "1",
doi = "10.1007/BF00690549",
language = "English (US)",
volume = "47",
pages = "213--221",
journal = "Acta Neuropathologica",
issn = "0001-6322",
publisher = "Springer Verlag",
number = "3",

}

TY - JOUR

T1 - Clioquinol and 2,5-hexanedione induce different types of distal axonopathy in the dog

AU - Krinke, G.

AU - Schaumburg, H. H.

AU - Spencer, Peter

AU - Thomann, P.

AU - Hess, R.

PY - 1979/1

Y1 - 1979/1

N2 - The central distal axonopathy induced in dogs by the administration of high doses of clioquinol is contrasted with the central-peripheral distal axonopathy precipitated by intoxication with 2,5-hexanedione. Mature, pure-bred Beagle dogs received a daily oral dose of 400 mg/kg of clioquinol for up to 7 months, or 1 ml per animal (approximately corresponding to 110 mg/kg) of 2,5-hexanedione for up to 5 months. Intoxicated and control animals were killed and perfused at monthly intervals, so that the spatial-temporal development of the lesion could be followed and correlated with clinical symptoms. During the treatment, dogs intoxicated with 2,5-hexanedione developed symptoms of peripheral neuropathy consisting of flaccid weakness, muscle atrophy, hind-limb foot-drop and areflexia. By contrast, the dogs surviving clioquinol intoxication exhibited a stiff-legged gait, hyperreflexia but no muscle atrophy. Light and electron microscope examination of central and peripheral nervous tissue from dogs intoxicated with 2,5-hexanedione revealed giant axonal swelling and distal axonal degeneration. By contrast, dogs receiving clioquinol showed a distal axonal degeneration confined to the optic tract and the long spinal cord tracts, without any visible involvement of peripheral nerves.

AB - The central distal axonopathy induced in dogs by the administration of high doses of clioquinol is contrasted with the central-peripheral distal axonopathy precipitated by intoxication with 2,5-hexanedione. Mature, pure-bred Beagle dogs received a daily oral dose of 400 mg/kg of clioquinol for up to 7 months, or 1 ml per animal (approximately corresponding to 110 mg/kg) of 2,5-hexanedione for up to 5 months. Intoxicated and control animals were killed and perfused at monthly intervals, so that the spatial-temporal development of the lesion could be followed and correlated with clinical symptoms. During the treatment, dogs intoxicated with 2,5-hexanedione developed symptoms of peripheral neuropathy consisting of flaccid weakness, muscle atrophy, hind-limb foot-drop and areflexia. By contrast, the dogs surviving clioquinol intoxication exhibited a stiff-legged gait, hyperreflexia but no muscle atrophy. Light and electron microscope examination of central and peripheral nervous tissue from dogs intoxicated with 2,5-hexanedione revealed giant axonal swelling and distal axonal degeneration. By contrast, dogs receiving clioquinol showed a distal axonal degeneration confined to the optic tract and the long spinal cord tracts, without any visible involvement of peripheral nerves.

KW - 2,5-hexanedione

KW - Clioquinol

KW - Distal axonopathy

KW - Dog

KW - Intoxication

UR - http://www.scopus.com/inward/record.url?scp=0018706243&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018706243&partnerID=8YFLogxK

U2 - 10.1007/BF00690549

DO - 10.1007/BF00690549

M3 - Article

VL - 47

SP - 213

EP - 221

JO - Acta Neuropathologica

JF - Acta Neuropathologica

SN - 0001-6322

IS - 3

ER -