Is turtle longevity linked to enhanced mechanisms for surviving brain anoxia and reoxygenation?

Exp Gerontol. 2003 Jul;38(7):797-800. doi: 10.1016/s0531-5565(03)00111-6.

Abstract

We suggest that the processes that protect the turtle brain against anoxia and subsequent reoxygenation might also contribute to turtle longevity since many of them are linked to age related neurodegeneration. In the turtle the mechanisms for conserving ion channel function are particularly robust. The anoxic turtle brain avoids excitatory neurotransmitter toxicity by maintaining a balance between dopamine and glutamate-release and still active uptake mechanisms. In the anoxic turtle brain the inhibitory tone is strengthened through a sustained rise in extracellular GABA, and a corresponding increase in the density of GABA(A) receptors. The turtle has enhanced mechanisms that protect against the formation of ROS and mechanisms to protect from ROS damage. As many of these may be selectively activated during anoxia and recovery, the turtle could serve as a useful model to identify and investigate mechanisms for activating key protection and rescue mechanisms implicated in aging.

MeSH terms

  • Adaptation, Physiological
  • Animals
  • Brain / metabolism*
  • Dopamine / metabolism
  • Glutamic Acid / metabolism
  • Hypoxia-Ischemia, Brain / metabolism*
  • Hypoxia-Ischemia, Brain / veterinary*
  • Ion Channels / metabolism
  • Longevity / physiology*
  • Reactive Oxygen Species / metabolism
  • Receptors, Dopamine / metabolism
  • Receptors, GABA-A / metabolism
  • Turtles / physiology*
  • gamma-Aminobutyric Acid / metabolism

Substances

  • Ion Channels
  • Reactive Oxygen Species
  • Receptors, Dopamine
  • Receptors, GABA-A
  • Glutamic Acid
  • gamma-Aminobutyric Acid
  • Dopamine