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. Author manuscript; available in PMC: 2013 Dec 16.
Published in final edited form as: Sci Transl Med. 2012 Oct 10;4(155):10.1126/scitranslmed.3004371. doi: 10.1126/scitranslmed.3004371

Fig. 6.

Fig. 6

HuCNS-SC–derived myelination in transplanted Shi-id mice. (A to F) HuCNS-SC–derived myelination resulted in a pronounced increase in the amount and distribution of the node of Ranvier-associated proteins, Caspr and Kv1.2, in cerebellar white matter. Data are from 8-week-old Shi-id mice [nontransplanted control (A to C); transplanted juvenile (D to F)]. The transition from the internal granule cell layer to the white matter is delineated with Hoechst fluorescent nuclear counterstain (blue) in (A) and (D). High-power image showing (C) restricted distribution of Caspr in a nontransplanted mouse and (F) a more diffuse distribution of Caspr in the paranodal region of axons in myelinated white matter of a transplanted mouse. (D and E) In transplanted animals, there was more Caspr (red) and Kv1.2 (green) staining in myelinated white matter compared to nontransplanted control animals (A and B). (G) Electron microscopic analysis of the cerebellar white matter of a nontransplanted Shi-id mice showing typical hypomyelination with a few loose myelin sheaths around axons. (H) Electron microscopic analysis of the cerebellar white matter of a Shi-id mouse brain 8 weeks after a HuCNS-SC transplant, showing host axons ensheathed with compact myelin derived from human oligodendrocytes. (I) Inset from (H) showing compact myelin with ~16 major dense lines. Magnifications, ×20,000 (G and H) and ×200,000 (I).