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Mitochondrial Depolarization in Glutamate-Stimulated Neurons: An Early Signal Specific to Excitotoxin Exposure
Open accessAbstract
A brief exposure to high concentrations of glutamate kills cultured forebrain neurons by an excitotoxic process that is dependent on Ca 2+influx through the NMDA receptor. In this study, we have measured striking changes in mitochondrial function during and immediately after intense glutamate receptor activation. Using indo-1 microfluorometry and a specific inhibitor of the mitochondrial Na+/Ca 2+exchanger, CGP-37157, we have demonstrated that mitochondria accumulate large quantities of Ca 2+during a toxic glutamate stimulus and further that Ca 2+efflux from mitochondria contributes to the prolonged [Ca 2+]i elevation after glutamate removal. We then used JC-1 (5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolocarbocyanine iodide), a ratiometric indicator of mitochondrial membrane potential (Δψ), to show that Ca 2+accumulation within the organelle dissipates Δψ. The abrupt loss of Δψ after glutamate stimulation did not occur in the presence of MK801 or in the absence of extracellular Ca 2+. The mitochondrial depolarization was also cyclosporin A-sensitive, indicating a probable role for the permeability transition pore. Hence mitochondrial Ca 2+accumulation and the subsequent permeability transition may be a critical early event specific to the NMDA receptor-mediated excitotoxic cascade.
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“…been proposed that these Ca 2ϩ -dependent changes in mitochondrial respiration allow excitable cells to couple ATP production with cellular activity (McCormack and Denton, 1993), and there is some evidence that mitochondrial function plays a role in synaptic plasticity (Nguyen and Atwood, 1994).”
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Metadata
- Authors
- White, R. J., & Reynolds, I. J.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1996-09-15
- Volume
- 16
- Issue
- 18
- Pages
- 5688-5697
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1550986239
- Cited by
- 592
- References
- 2
- FWCI
- 14.84
- Type
- journal article
- Language
- en
- Open access
- hybrid
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