Ej. Lehning et al., REOXYGENATION OF ANOXIC PERIPHERAL-NERVE MYELINATED AXONS PROMOTES REESTABLISHMENT OF NORMAL ELEMENTAL COMPOSITION, Brain research, 715(1-2), 1996, pp. 189-196
Previously we have shown that in vitro anoxia of rat peripheral nerve
myelinated axons causes sequential deregulation of axoplasmic Na, K an
d Ca; i.e., an initial influx of Na and loss of K is coupled to subseq
uent Ca accumulation [7]. In the present study, we examined the abilit
y of PNS axons to recover normal elemental composition following oxyge
n deprivation. Thus, electron probe X-ray microanalysis was used to de
termine the effects of post-anoxia reoxygenation on the concentrations
of elements (i.e., Na, K, Cl, Ca, Mg, P and S) in rat posterior tibia
l nerve myelinated axons and Schwann cells. Results indicate that foll
owing 180 min of anoxia, peripheral nerve reoxygenation (60 and 120 mi
n) promoted progressive recovery of normal elemental composition in ax
oplasm and mitochondria of small, medium and large diameter tibial ner
ve fibers. Our observations also indicate that small axons recovered n
ormal elemental concentrations more rapidly than larger counterparts.
Schwann cells and myelin exhibited only modest elemental disruption du
ring anoxia from which reoxygenation promoted full reparation. The abi
lity of peripheral nerve axons to restore normal elemental composition
during post-anoxia reoxygenation is in marked contrast to the exacerb
ation of elemental deregulation which ensued during in vitro reoxygena
tion of anoxic rat CNS fibers [14]. This differential response to reox
ygenation represents a fundamental difference in the pathophysiology o
f myelinated axons in the CNS and PNS.