In vivo analysis of glial cell phenotypes during a viral demyelinating disease in mice

(1 WPI) and were the only immunostained cells labeled at that time by a 2-h in vivo pulse of tritiated thymidine. Both GFAP+ only and GFAP+, 04+ astrocytes were also increased in the spinal cord at 1 WPI. Between two and four WPI, the infected spinal cord was characterized by the loss of (CNP+, 04+) oligodendrocytes within demyelinating lesions and the presence of O-2A progenitor cells and 04+, GFAP+ astrocytes, both of which could be labeled with thymidine. As remyelination proceeded, CNP immunostaining returned to near normal and tritiated thymidine injected previously during the demyelinating phase now appeared in CNP+ oligodendrocytes. Thus 04 positive O-2A progenitor cells proliferate early in the course of the demyelinating disease, while CNP positive oligodendrocytes do not. The timing of events suggests that the O-2A progenitors may give rise to new oligodendrocytes and to type 2 astrocytes, both of which are likely to be instrumental in the remyelination process. I s small rodents, regeneration of central nervous system (CNS) ~ myelin is often efficient after a demyelinating episode (reviewed in Ludwin, 1981) . In contrast, in multiple sclerosis, the paradigm of demyelinating diseases in human CNS, remyelination is often insufficient (reviewed in Silberberg, 1986) . Thus it appears important to elucidate the exact cellular and molecular events underlying CNS remyelination.