Mitochondrial membrane potential and ischemic neuronal death

Neurosci Res. 2006 Jul;55(3):234-43. doi: 10.1016/j.neures.2006.04.005. Epub 2006 May 22.

Abstract

Mitochondria are intracellular organelles in which high energy phosphate is produced. Ischemia causes depletion of the materials necessary to produce this phosphate and strongly affects the electron transport chain. Apoptosis commences during and after ischemia. As such, it is likely that a significant relationship exists between inactivation of electron transport and apoptosis. Mitochondrial membrane potential (MMP) reflects performance of the electron transport chain and can indicate a pathological disorder of this system. In an experimental setting, oxygen-glucose depletion (OGD) in neuronal cell culture has been employed to simulate an ischemic condition. The relationship between MMP and subsequent neuronal death during and after OGD has been examined. MMP dissipation and concomitant neuronal death have been reported, but recent studies have demonstrated mitochondrial hyperpolarization preceding neuronal death. The direction of MMP polarization depends on the extent of OGD. Long OGD results in depolarization, while shorter OGD induces hyperpolarization. Neurons are still viable during hyperpolarization, but the process may switch on the apoptotic cascade. Meanwhile, dissipation of MMP seems to be a consequence of severe energy deficit, leading to necrosis. MMP may be a marker of subsequent apoptosis, although a causal relationship remains to be determined.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Brain Infarction / metabolism*
  • Brain Infarction / physiopathology
  • Brain Ischemia / metabolism*
  • Brain Ischemia / physiopathology
  • Electron Transport / physiology
  • Energy Metabolism / physiology
  • Humans
  • Membrane Potentials / physiology
  • Mitochondrial Membranes / metabolism*
  • Nerve Degeneration / etiology
  • Nerve Degeneration / metabolism*
  • Nerve Degeneration / physiopathology
  • Signal Transduction / physiology