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A moderate but not total decrease of mitochondrial membrane potential triggers apoptosis in neuron-like cells.

I Gautier1, V Geeraert, J Coppey

  • 1Institut Jacques Monod, UMR 7592, CNRS, Universités P6/P7, Paris, France.

Neuroreport
|September 28, 2000
PubMed
Summary
This summary is machine-generated.

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A moderate decrease in mitochondrial membrane potential (mt delta psi) triggers apoptosis by affecting mitochondrial NADH and chromatin condensation. Complete collapse of mt delta psi, however, prevents these apoptotic events.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Neuroscience

Background:

  • Mitochondrial membrane potential (mt delta psi) is crucial for cellular energy production and apoptosis.
  • The precise role of varying degrees of mt delta psi perturbation in initiating apoptosis remains incompletely understood.

Purpose of the Study:

  • To investigate the impact of different levels of mitochondrial membrane potential (mt delta psi) disruption on the induction of apoptosis in neuron-like cells.
  • To elucidate the specific cellular events that follow partial versus complete dissipation of mt delta psi.

Main Methods:

  • Utilized intensified fluorescence digital-imaging microscopy to monitor mt delta psi in ND7 neuron-like cells.
  • Induced controlled perturbations of mt delta psi using carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) at varying concentrations and durations.

Related Experiment Videos

  • Assessed cellular responses including mitochondrial NADH levels, phosphatidylserine exposure, chromatin condensation, and mitochondrial morphology.

    • Main Results:

    • A moderate 40% decrease in mt delta psi (100 nM FCCP, 15 min) led to reduced mitochondrial NADH, phosphatidylserine exposure, and chromatin condensation in 36% of nuclei within 60 min.
    • Mitochondrial morphology was maintained during the moderate mt delta psi decrease and subsequent apoptotic events.
    • A rapid and total collapse of mt delta psi (10 microM FCCP, 60 min) did not induce chromatin condensation, suggesting a failure to initiate apoptosis.

    Conclusions:

    • Partial reduction of mitochondrial membrane potential (mt delta psi) is sufficient to initiate key apoptotic events, including chromatin condensation.
    • Sustained mitochondrial functions, enabled by a partial mt delta psi decrease, appear necessary for triggering apoptosis.
    • Complete and rapid dissipation of mt delta psi may inhibit or bypass the apoptotic pathway.