title: Mitochondrial permeability in neuronal death: possible relevance to the pathogenesis of Parkinson's disease.
abstract: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes catecholaminergic nerve cell loss and a syndrome similar to Parkinson's disease (PD). The metabolite of MPTP, MPP(+) (1-methyl-4-phenylpyridinium), decreases mitochondrial complex I activity similar to that in the PD nigra. Opening of a multi-protein, mitochondrial membrane pore constitutes a critical decisional event in some forms of apoptosis. We review recent findings showing that the permeability transition pore (PTP) opening caused by a decrease in the mitochondrial membrane potential (DeltaPsi(M)) contributes to MPP(+)-induced apoptosis. The reduction in DeltaPsi(M) appears to result from decreased proton pumping at complex I and therefore decreased complex I activity may also contribute to apoptosis in PD.
authors.affiliation: Department of Neurology, Mount Sinai School of Medicine, Annenburg 1470, P.O. Box 1137, One Gustave L. Levy Place, New York, NY, 10029-6574, USA.
authors.forename: W G
authors.initials: WG
authors.lastname: Tatton
authors.forename: R M
authors.initials: RM
authors.lastname: Chalmers-Redman
authors.forename: H J
authors.initials: HJ
authors.lastname: Rideout
authors.forename: N A
authors.initials: NA
authors.lastname: Tatton