Abstract:
:Inhibition of mitochondrial complex I is one of the leading hypotheses for dopaminergic neuron death associated with Parkinson's disease (PD). To test this hypothesis genetically, we used a mouse strain lacking functional Ndufs4, a gene encoding a subunit required for complete assembly and function of complex I. Deletion of the Ndufs4 gene abolished complex I activity in midbrain mesencephalic neurons cultured from embryonic day (E) 14 mice, but did not affect the survival of dopaminergic neurons in culture. Although dopaminergic neurons were more sensitive than other neurons in these cultures to cell death induced by rotenone, MPP(+), or paraquat treatments, the absence of complex I activity did not protect the dopaminergic neurons, as would be expected if these compounds act by inhibiting complex 1. In fact, the dopaminergic neurons were more sensitive to rotenone. These data suggest that dopaminergic neuron death induced by treatment with rotenone, MPP(+), or paraquat is independent of complex I inhibition.
journal_name
Proc Natl Acad Sci U S Aauthors
Choi WS,Kruse SE,Palmiter RD,Xia Zdoi
10.1073/pnas.0807581105subject
Has Abstractpub_date
2008-09-30 00:00:00pages
15136-41issue
39eissn
0027-8424issn
1091-6490pii
0807581105journal_volume
105pub_type
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