Elemental composition and water content of rat optic nerve myelinated axons and glial cells

Effects of in vitro anoxia and reoxygenation

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)6735-6746
Number of pages12
JournalJournal of Neuroscience
Volume15
Issue number10
StatePublished - 1995

Fingerprint

Optic Nerve
Neuroglia
Axons
Water
Myelin Sheath
In Vitro Techniques
Hypoxia
Reference Values
X-Rays
Electrons
Weights and Measures
Wounds and Injuries

Keywords

  • anoxia
  • axon injury
  • electron probe x-ray microanalysis
  • elements
  • glial cells
  • myelinated axons
  • Na-Ca exchanger
  • optic nerve
  • reperfusion

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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title = "Elemental composition and water content of rat optic nerve myelinated axons and glial cells: Effects of in vitro anoxia and reoxygenation",
abstract = "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.",
keywords = "anoxia, axon injury, electron probe x-ray microanalysis, elements, glial cells, myelinated axons, Na-Ca exchanger, optic nerve, reperfusion",
author = "LoPachin, {Richard M.} and Stys, {P. K.}",
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TY - JOUR

T1 - Elemental composition and water content of rat optic nerve myelinated axons and glial cells

T2 - Effects of in vitro anoxia and reoxygenation

AU - LoPachin, Richard M.

AU - Stys, P. K.

PY - 1995

Y1 - 1995

N2 - 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.

AB - 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.

KW - anoxia

KW - axon injury

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KW - Na-Ca exchanger

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KW - reperfusion

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