Home LiteratureArticle Details
PMID: 11145196 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Review

The neurotoxicant, cuprizone, as a model to study demyelination and remyelination in the central nervous system.

Brain pathology (Zurich, Switzerland) ·Vol. 11 ·No. 1 ·2001-01-00 ·Pages 107-16

Matsushima GK, Morell P

Abstract

Myelin of the adult CNS is vulnerable to a variety of metabolic, toxic, and autoimmune insults. That remyelination can ensue, following demyelinating insult, has been well demonstrated. Details of the process of remyelination are, however difficult to ascertain since in most experimental models of demyelination/remyelination the severity, localization of lesion site, or time course of the pathophysiology is variable from animal to animal. In contrast, an experimental model in which massive demyelination can be reproducibly induced in large areas of mouse brain is exposure to the copper chelator, cuprizone, in the diet. We review work from several laboratories over the past 3 decades, with emphasis on our own recent studies, which suggest an overall picture of cellular events involved in demyelination/remyelination. When 8 week old C57BL/6 mice are fed 0.2% cuprizone in the diet, mature olidgodendroglia are specifically insulted (cannot fulfill the metabolic demand of support of vast amounts of myelin) and go through apoptosis. This is closely followed by recruitment of microglia and phagoctytosis of myelin. Studies of myelin gene expression, coordinated with morphological studies, indicate that even in the face of continued metabolic challenge, oligodendroglial progenitor cells proliferate and invade demyelinated areas. If the cuprizone challenge is terminated, an almost complete remyelination takes place in a matter of weeks. Communication between different cell types by soluble factors may be inferred. This material is presented in the context of a model compatible with present data -- and which can be tested more rigorously with the cuprizone model. The reproducibility of the model indicates that it may allow for testing of manipulations (e.g. available knockouts or transgenics on the common genetic background, or pharmacological treatments) which may accelerate or repress the process of demyelination and or remyelination.

MeSH Terms
Animals Central Nervous System/drug effects Chelating Agents/pharmacology Cuprizone/pharmacology Demyelinating Diseases/physiopathology Mice Mice, Inbred C57BL Microglia Models, Animal Myelin Sheath Oligodendroglia/physiology
Chemicals
Chelating Agents Cuprizone
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Matsushima G K
UNC Neuroscience Center, Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, 27599, USA. gkmats@med.unc.edu
Morell P
References (44)
44 references, click to expand
  1. Experimental allergic encephalomyelitis. Antiserum inhibition of myelination in vitro.
    Lab Invest. 1970 Nov;23(5):536-42 PMID: 5483885
  2. Demyelination of the superior cerebellar peduncle in the mouse induced by cuprizone.
    J Neurol Sci. 1973 Sep;20(1):63-72 PMID: 4744511
  3. Unsuccessful attempts to produce disease with tissues from mice fed on a diet containing cuprizone.
    Res Vet Sci. 1973 Jan;14(1):128-30 PMID: 4736048
  4. Macrophage recruitment in different models of nerve injury: lysozyme as a marker for active phagocytosis.
    J Neurosci Res. 1995 Jan 1;40(1):99-107 PMID: 7714930
  5. An immunohistochemical study of myelin proteins during remyelination in the central nervous system.
    Acta Neuropathol. 1984;63(3):240-8 PMID: 6205535
  6. Trace elements in nutrition for premature infants.
    Clin Perinatol. 1995 Mar;22(1):223-40 PMID: 7781254
  7. Atypical localization of the oligodendrocytic isoform (PI) of glutathione-S-transferase in astrocytes during cuprizone intoxication.
    J Neurosci Res. 1993 Oct 1;36(2):183-90 PMID: 8263971
  8. Chronic demyelination inhibits remyelination in the central nervous system. An analysis of contributing factors.
    Lab Invest. 1980 Oct;43(4):382-7 PMID: 7442125
  9. Copper: not too little, not too much, but just right. Based on the triennial Pewterers Lecture delivered at the National Hospital for Neurology, London, on 23 March 1995.
    J R Coll Physicians Lond. 1995 Jul-Aug;29(4):280-8 PMID: 7473321
  10. Observations on oligodendrocyte degeneration, the resolution of status spongiosus and remyelination in cuprizone intoxication in mice.
    J Neurocytol. 1972 Dec;1(4):413-26 PMID: 8530973
  11. Gene expression in brain during cuprizone-induced demyelination and remyelination.
    Mol Cell Neurosci. 1998 Nov;12(4-5):220-7 PMID: 9828087
  12. Giant hepatic mitochondria: production in mice fed with cuprizone.
    Science. 1969 Jan 3;163(3862):81-2 PMID: 5763494
  13. The neurotoxicant, cuprizone, retards the differentiation of oligodendrocytes in vitro.
    J Neurol Sci. 1999 Oct 15;168(2):116-20 PMID: 10526193
  14. Histopathologic and enzyme histochemical observations of the cuprizone-induced brain edema.
    Exp Mol Pathol. 1971 Aug;15(1):82-96 PMID: 4254498
  15. Spongiform encephalopathy induced in rats and guinea pigs by cuprizone.
    Exp Mol Pathol. 1969 Jun;10(3):274-87 PMID: 5788627
  16. Effects of carbonic anhydrase II (CAII) deficiency on CNS structure and function in the myelin-deficient CAII-deficient double mutant mouse.
    J Neurosci Res. 1995 Mar 1;40(4):451-7 PMID: 7616606
  17. Blood-brain barrier permeability to horseradish peroxidase in twitcher and cuprizone-intoxicated mice.
    Brain Res. 1987 Nov 3;425(1):186-90 PMID: 3427420
  18. Central nervous system demyelination and remyelination in the mouse: an ultrastructural study of cuprizone toxicity.
    Lab Invest. 1978 Dec;39(6):597-612 PMID: 739762
  19. Reactive microgliosis.
    Prog Neurobiol. 1999 Apr;57(6):563-81 PMID: 10221782
  20. Interferon-gamma protects against cuprizone-induced demyelination.
    Mol Cell Neurosci. 2000 Oct;16(4):338-49 PMID: 11085872
  21. Central nervous system remyelination: studies in chronically damaged tissue.
    Ann Neurol. 1994;36 Suppl:S143-5 PMID: 8017878
  22. Blood-brain barrier permeability during Cuprizone-induced demyelination. Implications for the pathogenesis of immune-mediated demyelinating diseases.
    J Neurol Sci. 1987 Apr;78(2):125-37 PMID: 3553434
  23. Insulin-like growth factor I gene expression is induced in astrocytes during experimental demyelination.
    Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1894-8 PMID: 1371885
  24. Enzymic activities and sodium, potassium and copper concentrations in mouse brain and liver after cuprizone treatment in vivo.
    J Neurochem. 1973 Nov;21(5):1147-51 PMID: 4357499
  25. Variation in the response of mice to cuprizone.
    Res Vet Sci. 1973 May;14(3):385-7 PMID: 4805158
  26. An autoradiographic study of cellular proliferation in remyelination of the central nervous system.
    Am J Pathol. 1979 Jun;95(3):683-96 PMID: 453329
  27. Insulin-like growth factor-1 inhibits mature oligodendrocyte apoptosis during primary demyelination.
    J Neurosci. 2000 Aug 1;20(15):5703-8 PMID: 10908609
  28. Remyelination of the superior cerebellar peduncle in old mice following demyelination induced by cuprizone.
    J Neurol Sci. 1974 May;22(1):121-6 PMID: 4830551
  29. Cuprizone neurotoxicity in the rat: morphologic observations.
    J Neurol Sci. 1988 Apr;84(2-3):223-37 PMID: 2837540
  30. Decrease in oligodendrocyte carbonic anhydrase activity preceding myelin degeneration in cuprizone induced demyelination.
    J Neurol Sci. 1987 Jun;79(1-2):141-8 PMID: 2440995
  31. Status spongiosus of CNS and hepatic changes induced by cuprizone (biscyclohexanone oxalyldihydrazone).
    Am J Pathol. 1969 Feb;54(2):307-25 PMID: 5765567
  32. Co-localization of NG2 proteoglycan and PDGF alpha-receptor on O2A progenitor cells in the developing rat brain.
    J Neurosci Res. 1996 Feb 01;43(3):299-314 PMID: 8714519
  33. Mature oligodendrocyte apoptosis precedes IGF-1 production and oligodendrocyte progenitor accumulation and differentiation during demyelination/remyelination.
    J Neurosci Res. 2000 Aug 1;61(3):251-62 PMID: 10900072
  34. Central nervous system remyelination clinical application of basic neuroscience principles.
    Brain Pathol. 1996 Jul;6(3):331-44 PMID: 8864288
  35. Parameters related to lipid metabolism as markers of myelination in mouse brain.
    J Neurochem. 2001 Jan;76(1):77-86 PMID: 11145980
  36. Phagocytosis of myelin in demyelinative disease: a review.
    Neurochem Res. 1999 Feb;24(2):261-8 PMID: 9972873
  37. Studies on the induction of hydrocephalus and spongy degeneration by cuprizone feeding and attempts to antidote the toxicity.
    Life Sci. 1967 Jan 1;6(1):11-9 PMID: 6030552
  38. The response of oligodendrocytes to chemical injury.
    Acta Neurol Scand Suppl. 1984;100:33-8 PMID: 6385605
  39. Clinical and histological observations on cuprizone toxicity and scrapie in mice.
    Res Vet Sci. 1971 Jul;12(4):378-80 PMID: 5105163
  40. Biochemical changes in Cuprizone-induced spongiform encephalopathy. I. Changes in the activities of 2',3'-cyclic nucleotide 3'-phosphohydrolase, oligodendroglial ceramide galactosyl transferase, and the hydrolysis of the alkenyl group of alkenyl, acyl-glycerophospholipids by plasmalogenase in different regions of the brain.
    Neurochem Res. 1983 Aug;8(8):1029-44 PMID: 6312351
  41. Microglial/macrophage accumulation during cuprizone-induced demyelination in C57BL/6 mice.
    J Neuroimmunol. 1998 Dec 1;92(1-2):38-49 PMID: 9916878
  42. Remyelination of the superior cerebellar peduncle in the mouse following demyelination induced by feeding cuprizone.
    J Neurol Sci. 1973 Sep;20(1):73-83 PMID: 4744512
  43. Induction of myelin-associated glycoprotein mRNA in experimental remyelination.
    Brain Res. 1990 Apr 9;513(1):152-5 PMID: 1693539
  44. A pi form of glutathione-S-transferase is a myelin- and oligodendrocyte-associated enzyme in mouse brain.
    J Neurochem. 1991 Jul;57(1):95-102 PMID: 1711102
Article Info
Journal
Brain pathology (Zurich, Switzerland)
Abbr.
Brain Pathol
ISSN
1015-6305
Published
2001-01-00
Pages
107-16
Language
English
Region
Switzerland
NLM ID
9216781
PMCID
PMC8098267
Subset
IM
Grants
NINDS NIH HHS · NS11615 · United States
NINDS NIH HHS · NS35372 · United States
NINDS NIH HHS · NS37815 · United States
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: product@genelibs.com