Figure 1.

Clinical, serological, and morphological features of AMAN rabbits. A, Clinical course of each paralyzed rabbit. Eight rabbits were divided into three groups: Bg-16, Bg-17, and Bg-18 at acute progressive phase (within a few days after the neurological onset); Bg-19 and Bg-20 at early recovery phase (∼2 weeks after the onset); Bg-21, Bg-22, and Bg-23 at late recovery phase (>4 weeks after the onset). B, Thin-layer chromatography with immunostaining. Lane 1, Bovine brain ganglioside mixture; lane 2, ganglioside mixture extracted from rabbit peripheral nerves. Plasma IgG obtained from AMAN rabbits Bg-16, Bg-17, and Bg-18 strongly react with GM1 from both bovine brain and rabbit peripheral nerve. IgG from Bg-16 and Bg-18 also weakly bind to GD1b. The immunostaining patterns of IgG from paralyzed rabbits are similar to IgG from a patient with AMAN. Anti-GM1 mAb (GB2) reacts strongly and specifically to GM1. C, D, Electron microscopy showing lengthened nodes in ventral roots from a rabbit 2 d after onset (C) and Bg-20 at the early recovery phase (D). Schwann cell cytoplasm expands forming bulb-like structure filled with mitochondria. No typical microvilli of Schwann cells are obvious. E, Higher magnification of the boxed area in D. Some paranodal loops (arrowheads) are detached from axonal membrane. Scale bars: C, 5 μm; D, 2 μm; E, 0.2 μm.