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, Peter K.
PY - 1995/10
Y1 - 1995/10
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 - Na-Ca exchanger
KW - anoxia
KW - axon injury
KW - electron probe x-ray microanalysis
KW - elements
KW - glial cells
KW - myelinated axons
KW - optic nerve
KW - reperfusion
UR - http://www.scopus.com/inward/record.url?scp=0028862233&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028862233&partnerID=8YFLogxK
U2 - 10.1523/jneurosci.15-10-06735.1995
DO - 10.1523/jneurosci.15-10-06735.1995
M3 - Article
C2 - 7472432
AN - SCOPUS:0028862233
SN - 0270-6474
VL - 15
SP - 6735
EP - 6746
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 10
ER -