Reactive gliosis has been considered to be the major cause of regenera
tive failure of the mature mammalian central nervous system (CNS). It
is classically defined by increased glial fibrillary acidic protein ex
pression. However, the response to injury is not uniform throughout th
e CNS. This heterogeneity is becoming more apparent as other markers f
or reactive astrocytes emerge from recent studies. These molecules may
be more relevant markers of the functional state of reactive astrocyt
es and may help us understand the events leading to failure of regener
ation in the CNS.