Decrease in oligodendrocyte carbonic anhydrase activity preceding myelin degeneration in cuprizone induced demyelination
- PMID: 2440995
- DOI: 10.1016/0022-510x(87)90268-1
Decrease in oligodendrocyte carbonic anhydrase activity preceding myelin degeneration in cuprizone induced demyelination
Abstract
Both immunohistochemical and biochemical evidence is presented to show for the first time that carbonic anhydrase II (CA II) activity falls in the brain of mice in cuprizone (bis(cyclohexanone)oxalyldihydrazone) induced demyelination well before demyelination develops. This fall began during the first week, whereas the first signs of myelin degeneration induced by cuprizone did not appear until 3 weeks and demyelination in the superior cerebellar peduncle in the mouse took 6-8 weeks to develop. The findings suggest that oligodendrocyte CA II activity is essential either for the survival of oligodendrocytes or for the maintenance of central myelin.
Similar articles
-
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. doi: 10.1002/jnr.490360208. J Neurosci Res. 1993. PMID: 8263971
-
Experimental demyelination caused by primary oligodendrocyte dystrophy. Regional distribution of the lesions in the nervous system of mice [corrected].Ideggyogy Sz. 2005 Jan 20;58(1-2):40-3. Ideggyogy Sz. 2005. PMID: 15884397
-
Cuprizone-induced demyelination in the rat cerebral cortex and thyroid hormone effects on cortical remyelination.Exp Neurol. 2012 May;235(1):357-67. doi: 10.1016/j.expneurol.2012.02.018. Epub 2012 Mar 7. Exp Neurol. 2012. PMID: 22421533
-
Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Mol Neurodegener. 2022 May 7;17(1):34. doi: 10.1186/s13024-022-00538-8. Mol Neurodegener. 2022. PMID: 35526004 Free PMC article. Review.
-
The response of oligodendrocytes to chemical injury.Acta Neurol Scand Suppl. 1984;100:33-8. Acta Neurol Scand Suppl. 1984. PMID: 6385605 Review.
Cited by
-
Short-term cuprizone feeding induces selective amino acid deprivation with concomitant activation of an integrated stress response in oligodendrocytes.Cell Mol Neurobiol. 2013 Nov;33(8):1087-98. doi: 10.1007/s10571-013-9975-y. Epub 2013 Aug 25. Cell Mol Neurobiol. 2013. PMID: 23979168 Free PMC article.
-
Conditional Deletion of the L-Type Calcium Channel Cav1.2 in NG2-Positive Cells Impairs Remyelination in Mice.J Neurosci. 2017 Oct 18;37(42):10038-10051. doi: 10.1523/JNEUROSCI.1787-17.2017. Epub 2017 Sep 12. J Neurosci. 2017. PMID: 28899915 Free PMC article.
-
Revisiting the Pathoetiology of Multiple Sclerosis: Has the Tail Been Wagging the Mouse?Front Immunol. 2020 Sep 29;11:572186. doi: 10.3389/fimmu.2020.572186. eCollection 2020. Front Immunol. 2020. PMID: 33117365 Free PMC article. Review.
-
The neurotoxicant, cuprizone, as a model to study demyelination and remyelination in the central nervous system.Brain Pathol. 2001 Jan;11(1):107-16. doi: 10.1111/j.1750-3639.2001.tb00385.x. Brain Pathol. 2001. PMID: 11145196 Free PMC article. Review.
-
mTOR Signaling Regulates Metabolic Function in Oligodendrocyte Precursor Cells and Promotes Efficient Brain Remyelination in the Cuprizone Model.J Neurosci. 2021 Oct 6;41(40):8321-8337. doi: 10.1523/JNEUROSCI.1377-20.2021. Epub 2021 Aug 20. J Neurosci. 2021. PMID: 34417330 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Miscellaneous