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- W2180091405 abstract "The mechanisms underlying neuronal death following excessive activity such as occurs during prolonged seizures are unclear, but mitochondrial dysfunction has been hypothesised to play a role. Here, we tested this with fluorescence imaging techniques in rat glio-neuronal neocortical co-cultures using low Mg 2+ levels to induce seizure-like activity. Glutamate activation of NMDA receptors resulted in Ca 2+ oscillations in neurons and a sustained depolarisation of the mitochondrial membrane potential, which was cyclosporine A sensitive, indicating mitochondrial permeability and transition pore opening. It was also dependent on glutamate release and NMDA receptor activation, because depolarisation was not observed after depleting vesicular glutamate with vacuolar-type H + -ATPase concanamycin A or blocking NMDA receptors with APV. Neuronal ATP levels in soma and dendrites decreased significantly during prolonged seizures and correlated with the frequency of the oscillatory Ca 2+ signal, indicative of activity-dependent ATP consumption. Blocking mitochondrial complex I, complex V or uncoupling mitochondrial oxidative phosphorylation under low-Mg 2+ conditions accelerated activity-dependent neuronal ATP consumption. Neuronal death increased after two and 24 hours of low Mg 2+ levels compared with control treatment, and was reduced by supplementation with the mitochondrial complex I substrate pyruvate. These findings demonstrate a crucial role for mitochondrial dysfunction in seizure-activity-induced neuronal death, and that strategies aimed at redressing this are neuroprotective." @default.
- W2180091405 created "2016-06-24" @default.
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- W2180091405 date "2011-10-01" @default.
- W2180091405 modified "2023-09-27" @default.
- W2180091405 title "PROLONGED SEIZURE ACTIVITY IMPAIRS MITOCHONDRIAL BIOENERGETICS AND INDUCES CELL DEATH" @default.
- W2180091405 hasPublicationYear "2011" @default.
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