Does astrocytic glycogen benefit axon function and survival in CNS white matter during glucose deprivation?

Does astrocytic glycogen benefit axon function and survival in CNS white matter during glucose... Axons, the functional elements in CNS white matter, are frequently injured by ischemia, especially in the context of stroke. The pathophysiology of axonal injury induced by energy deprivation has been analyzed in the rat optic nerve and involves excessive calcium influx by way of reverse Na+/Ca2+ exchange and Ca2+ channels. Evidence is presented that CNS axonal function can be supported in the absence of glucose by intrinsic energy reserves provided through the breakdown of astrocytic glycogen. It is argued that energy is transferred from astrocytes to axons in the form of lactate, which is able to maintain axonal function when substituted for glucose. These observations complement the increasingly convincing hypothesis that astrocytes and neurons interact metabolically, both in the course of normal activity and under pathological conditions such as ischemia. The emerging picture would be no surprise to Camillo Golgi, who predicted a close facsimile of this glial‐neuronal interaction more than a century ago. GLIA 21:134–141, 1997. © 1997 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Glia Wiley

Does astrocytic glycogen benefit axon function and survival in CNS white matter during glucose deprivation?

Glia, Volume 21 (1) – Sep 1, 1997

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Publisher
Wiley
Copyright
Copyright © 1997 Wiley‐Liss, Inc.
ISSN
0894-1491
eISSN
1098-1136
D.O.I.
10.1002/(SICI)1098-1136(199709)21:1<134::AID-GLIA15>3.0.CO;2-T
Publisher site
See Article on Publisher Site

Abstract

Axons, the functional elements in CNS white matter, are frequently injured by ischemia, especially in the context of stroke. The pathophysiology of axonal injury induced by energy deprivation has been analyzed in the rat optic nerve and involves excessive calcium influx by way of reverse Na+/Ca2+ exchange and Ca2+ channels. Evidence is presented that CNS axonal function can be supported in the absence of glucose by intrinsic energy reserves provided through the breakdown of astrocytic glycogen. It is argued that energy is transferred from astrocytes to axons in the form of lactate, which is able to maintain axonal function when substituted for glucose. These observations complement the increasingly convincing hypothesis that astrocytes and neurons interact metabolically, both in the course of normal activity and under pathological conditions such as ischemia. The emerging picture would be no surprise to Camillo Golgi, who predicted a close facsimile of this glial‐neuronal interaction more than a century ago. GLIA 21:134–141, 1997. © 1997 Wiley‐Liss, Inc.

Journal

GliaWiley

Published: Sep 1, 1997

References

  • The perinodal astrocyte
    Black, Black; Waxman, Waxman
  • Voltage‐gated calcium channels in CNS white matter: Role in anoxic injury
    Fern, Fern; Ransom, Ransom; Waxman, Waxman
  • In vivo location of the rate‐limiting step of hexose uptake in muscle and brain tissue of rats
    Furler, Furler; Jenkins, Jenkins; Storlien, Storlien; Kraegen, Kraegen
  • Effects of anoxia on ion distribution in brain
    Hansen, Hansen
  • The physiology of glial cells
    Kuffler, Kuffler; Nicholls, Nicholls
  • Nervenkitt: Notes on the history of the concept of neuroglia
    Somjen, Somjen
  • Simulation of aspects of ischemia in cell culture: Changes in lactate compartmentation
    Walz, Walz; Mukerji, Mukerji
  • Uptake of radioactive glucose and its conversion to glycogen by neurons and glial cells in the leech central nervous system
    Wolfe, Wolfe; Nicholls, Nicholls
  • Alterations in reactive oxygen, pH, and calcium in astrocytoma cells during lethal injury
    Yankuan, Yankuan; Taylor, Taylor; Sun, Sun

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