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.
Glia – Wiley
Published: Sep 1, 1997
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