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everal distinct cell types in the adult central nervous
+ c) _2 l' U9 F1 }/ U7 t8 V tsystem have been suggested to act as stem or prog-
; k6 q/ N+ W, penitor cells generating new cells under physiological
" d6 c# _+ R( ]5 V" n. uor pathological conditions. We have assessed the5 |, _/ Z' _) \% k+ ?" |& `8 l0 e. U
origin of new cells in the adult mouse spinal cord by& |* h' p: f3 [
genetic fate mapping. Oligodendrocyte progenitors- `4 ^- Z: v; Q0 V/ m# v) s
self-renew, give rise to newmature oligodendrocytes,
: C) H( D4 B- y& T# Gand constitute the dominating proliferating cell popu-
9 A6 @# M; e$ flation in the intact adult spinal cord. In contrast, astro-& P5 _. k4 |; ?; X/ q
cytes and ependymal cells, which are restricted to
/ k5 ]+ F8 k& P) ]limited self-duplication in the intact spinal cord,+ _* m3 _& A+ t6 h+ M3 m
generate the largest number of cells after spinal cord
; b* P) d( v7 L+ ]1 rinjury. Only ependymal cells generate progeny of
, {5 a$ q# ^/ K* p Dmultiple fates, and neural stemcell activity in the intact
- Q* s5 \0 \4 z& B# ^4 h+ ]! t* Eand injured adult spinal cord is confined to this cell
( B2 y; l/ e3 p5 F# C2 [population. We provide an integrated view of how
8 d8 L; g- |4 R6 s4 u1 Oseveraldistinct cell types contribute in complementary2 Q# e q5 x2 q+ l
ways to cell maintenance and the reaction to injury. |
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