Rapid alterations of the axon membrane in antibody‐mediated demyelination

Abstract

Alterations of nodal and paranodal axolemma of the rat sciatic nerve were investigated in antigalactocerebroside serum-induced demyelination. A ferric ion-ferrocyanide (FeFCN) stain that appears to stain the regions with a high sodium channel density in nerve fibers was applied. When acute conduction block was initiated 20 to 180 minutes after the antiserum injection, myelin terminal loops began to be detached from the paranodal axolemma and reaction product of FeFCN stain originally localized at the nodes decreased in density and extended to the paranodal axolemma. By the time that complete conduction block was established, 5 hours after the injection, FeFCN stain was barely detectable around the nodal area. The loss of staining was associated with detachment and vesiculovacuolar degeneration of the paranodal myelin. This rapid deterioration and disappearance of normal cytochemical characteristics of the axolemma in the presence of only modest paranodal demyelination could be a morphological correlate of the loss of excitability of the axon membrane.

The effects of aerobic exercise training on the age-related lipid peroxidation, Schwann cell apoptosis and ultrastructural changes in the sciatic nerve of rats

“…Loss of contact between paranodal SC loops/myelin and axolemma has been reported with aging (Hinman et al, 2006;Sugiyama et al, 2002) and other pathologic conditions (Chang et al, 1994;Saida et al, 1984;Ho and Yu, 1989). However, exercise training abolished these effects and in fact, the myelin sheath was thickened and had frequent folding with outward and inward protrusions in the ET group.…”

Axo-glial dysjunction. A novel structural lesion that accounts for poorly reversible slowing of nerve conduction in the spontaneously diabetic bio-breeding rat.

“…Alternatively, axo-glial dysjunction may reflect independent underlying biochemical abnormalities that may or may not be involved in the earlier reversible conduction slowing and paranodal swelling. Galactocerebroside, a lipid element in axo-glial junctions (37), is depleted from myelin isolated from the BB rat (38). Membrane glycolipids are further implicated in chronic conduction slowing by studies in the spontaneously diabetic db/ db mouse, where ganglioside treatment selectively improves nerve conduction during the structural phase of diabetic neuropathy (39).…”

Rapid and reversible responses to IVIG in autoimmune neuromuscular diseases suggest mechanisms of action involving competition with functionally important autoantibodies

“…They also showed that acute conduction block was associated with a striking reduction in the normally dense staining of Na + channels in the nodes of Ranvier, at a time when only minimal paranodal demyelination was visible. Thus, the rapid disappearance of the normal architecture in the node, rather than demyelination per se , was considered the morphologic correlate of the loss of axonal excitability (Saida et al ., ) . Yuki drew similar conclusions about axonal damage and degeneration without demyelination from serial studies of patients with AMAN, and from injecting their IgG into rat sciatic nerves (Yuki et al ., ) .…”