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mammals in which a “glial scar” blocks the passage of incoming axons (Ramón y
Cajal 1913 ; Silver and Miller 2004 ; Thuret et al. 2006 ). Studies made on lizards
(Egar et al. 1970 ), tailed amphibians (Singer et al. 1979 ; Zhang et al. 2000 ;
McHedlishvili et al. 2007 ) and immature eels (Dervan and Roberts 2003 ) have
shown that regeneration of the injured spinal cord is orchestrated by the plastic reac-
tion of ependymal cells. One of the major events after injury in species with and
without endogenous repair capabilities is an increase in the proliferation of ependy-
mal cells (Mothe and Tator 2005 ; Meletis et al. 2008 ). In turtles, the proliferative
reaction is spatially focused around the lesion epicenter engaging mostly the
domains of BLBP/Pax6 progenitors (Rehermann et al. 2011 ). The capability of RG
expressing BLBP to contribute to neural repair has been demonstrated in rodents in
which transplanted embryonic RG “bridge spinal cord lesions and promote func-
tional recovery” (Hasegawa et al. 2004 ). The presence of BLBP cells within the
Fig. 5.6 Cartoon showing the possible involvement of P2X7 receptors and Ca2+ waves in the
reaction of CC-contacting prgenitors after spinal cord injury. Putative mechanisms are proposed
N. Marichal et al.