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Journal of Neuroscience, Vol 15, 6735-6746, Copyright © 1995 by Society for Neuroscience
Elemental composition and water content of rat optic nerve myelinated axons and glial cells: effects of in vitro anoxia and reoxygenation
RM LoPachin Jr and PK Stys
Department of Anesthesiology, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, New York 10467-2490, USA.
Electron probe x-ray microanalysis was used to measure water content and
concentrations (mmol/kg dry weight) of elements (Na, P, S, Cl, K, Ca, and
Mg) in myelinated axons and glial cells of rat optic nerve exposed to in
vitro anoxia and reoxygenation. In response to anoxia, large, medium, and
small diameter fibers exhibited an early (5 min) and progressive loss of Na
and K regulation which culminated (60 min) in severe depletion of
respective transmembrane gradients. As axoplasmic Na levels increased
during anoxic exposure, a parallel rise in Ca content was noted. For all
axons, mean water content decreased progressively during the initial 10 min
of anoxia and then returned toward normal values as anoxia continued.
Analyses of mitochondrial areas revealed a similar pattern of elemental
disruption except that Ca concentrations rose more rapidly during anoxia.
Following 60 min of postanoxia reoxygenation, the majority of larger fibers
displayed little evidence of recovery, whereas a subpopulation of small
axons exhibited a trend toward restoration of normal elemental composition.
Glial cells and myelin were only modestly affected by anoxia and subsequent
reoxygenation. Thus, anoxic injury of CNS axons is associated with
characteristic changes in axoplasmic distributions of Na, K, and Ca. The
magnitude and temporal patterns of elemental Na and Ca disruption are
consistent with reversal of Na(+)-Ca2+ exchange and subsequent Ca entry
(Stys et al., 1992). During reoxygenation, elemental deregulation continues
for most CNS fibers, although a subpopulation of small axons appears to be
capable of recovery.
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