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Roles of glucose in photoreceptor survival

Andrei O Chertov1, Lars Holzhausen, Iok Teng Kuok

  • 1Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA.

The Journal of Biological Chemistry
|August 16, 2011
PubMed

Insights

Glucose deprivation in mouse photoreceptors reveals two cell death phases. Reduced mitochondrial activity causes rapid death, while slower death stems from a need for cellular repair substrates.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Metabolism

Background:

  • Vertebrate photoreceptor neurons possess high metabolic energy demands.
  • Photoreceptor viability is highly sensitive to genetic and environmental stressors.

Purpose of the Study:

  • To investigate the link between energy metabolism and cell death in mouse photoreceptors.
  • To evaluate the metabolic effects of glucose deprivation on photoreceptor viability.

Main Methods:

  • Assessed oxygen consumption, lactate production, ATP, NADH/NAD+ ratios, and TCA cycle intermediates.
  • Monitored morphological changes, autophagy, and cell viability in mouse retinas.
  • Compared retinas with glucose, without glucose, and with mitochondrion-specific fuels.

Main Results:

  • Identified distinct rapid and slow phases of photoreceptor cell death.
  • The rapid phase correlated with decreased mitochondrial activity.
  • The slower phase indicated a requirement for substrates for cell maintenance and repair.

Conclusions:

  • Glucose is critical for photoreceptor energy metabolism and survival.
  • Photoreceptor death involves both immediate energy depletion and longer-term substrate needs.
  • Mitochondrial function is essential for rapid photoreceptor survival.

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