Distribution of oligodendrocyte loss and mitochondrial toxicity in the cuprizone-induced experimental demyelination model

作者：Acs P^*; Selak M A; Komoly S; Kalman B

来源：Journal of Neuroimmunology, 2013, 262(1-2): 128-131.

DOI：10.1016/j.jneuroim.2013.06.012

• Cuprizone
• Copper chelation
• Mitochondrial toxicity
• Demyelination
• Selective vulnerability
• Multiple sclerosis

Cuprizone is a copper-chelating mitochondrial toxin that causes oligodendrocyte apoptosis and demyelination preferentially in the corpus callosum (CC) and the superior cerebellar peduncles, but not in the spinal cord (SC) of C57BL/6 mice. Here we aimed to determine the activities of copper-containing enzymes in correlation with the distribution of demyelination during exposure to cuprizone. The study revealed mitochondrial complex IV and superoxide dismutase activity alterations in both the pathology-affected CC and the non-affected SC. This observation raises the possibility that regionally different subcellular molecular interactions lead to the selective oligodendrocyte loss induced by the nonselective mitochondrial toxin, cuprizone.

• 出版日期2013-9-15