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Journal Article

Mitochondrial permeability transition can be directly monitored in living neurons

MPS-Authors

Gillessen,  T
Max Planck Institute of Psychiatry, Max Planck Society;

Grasshoff,  C
Max Planck Institute of Psychiatry, Max Planck Society;

Szinicz,  L
Max Planck Institute of Psychiatry, Max Planck Society;

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Gillessen, T., Grasshoff, C., & Szinicz, L. (2002). Mitochondrial permeability transition can be directly monitored in living neurons. Biomedicine & Pharmacotherapy, 56(4), 186-193.


Cite as: http://hdl.handle.net/11858/00-001M-0000-000E-A1DD-0
Abstract
Mitochondria have been suggested as key players in apoptotic cell death of neurons and many other tissues, since the release of proapoptotic molecules from mitochondria is implicated in caspase activation. As a potential release mechanism, the occurrence of a large pore opening in the inner membrane (mitochondrial permeability transition pore, PTP) has been proposed, but has not yet been observed directly in neurons. We investigated whether the calceln/Co2+-quenching technique introduced by Petronilli et al. [Biofactors 8 (1998) 263], which allows direct observation of PTP opening, car. be applied to neurons. Exposure of calcein-loaded neurons to Co2+ ions resulted in the fading of diffuse cytoplasmic calcein fluorescence, with organelle-restricted fluorescent spots remaining. These spots were colocalized with mitochondrially- entrapped tetramethylrhodamineethylester (TMRE) fluorescence and corresponded to colocalization of calcein and TMRE fluorescence in digitonin-permeabilized neurons. Importantly, extensive neuronal calcium loading, which is assumed to induce PTP opening, resulted in significant fading of mitochondrial fluorescence, suggesting the occurrence of permeability transition. This fluorescence decrease could be completely prevented by the PTP blocker cyclosporin A. (C) 2002 Editions scientifiques et medicales Elsevier SAS