Mitochondrial complex IV is lost in neurons in the cuprizone mouse model.
Mitochondrion
; 50: 58-62, 2020 01.
Article
em En
| MEDLINE
| ID: mdl-31678601
ABSTRACT
BACKGROUND:
Cuprizone administration in mice leads to oligodendrocyte death and demyelination. The effect is thought to reflect copper-chelation that leads to inhibition of complex IV of the mitochondrial respiratory chain. The effects this drug has on neurons are less well known.OBJECTIVE:
To investigate the toxic effects of cuprizone on mitochondria in neurons.METHODS:
Male c57Bl/6 mice were fed 0.2% cuprizone for up to 5â¯weeks. Cuprizone-fed and control mice were examined at week 1, 3, 5 and 4â¯weeks after cessation of cuprizone exposure. The brain was examined for myelin, complex I, complex IV and for COX/SDH activities. Mitochondrial-DNA was investigated for deletions and copy number variation.RESULTS:
We found decreased levels of complex IV in the cerebellar Purkinje neurons of mice exposed to cuprizone. This decrease was not related to a general decrease in mitochondrial volume or mass, as there were no differences in the levels of complex I or TOMM20.CONCLUSION:
Neurons are affected by cuprizone-treatment. Whether this mitochondrial dysfunction acts as a subclinical trigger for demyelination and the long-term axonal degeneration that proceeds after cuprizone treatment stops remains unclear.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Contexto em Saúde:
6_ODS3_enfermedades_notrasmisibles
Base de dados:
MEDLINE
Assunto principal:
Células de Purkinje
/
Complexo IV da Cadeia de Transporte de Elétrons
/
Cuprizona
Limite:
Animals
Idioma:
En
Revista:
Mitochondrion
Ano de publicação:
2020
Tipo de documento:
Article