Is reactive gliosis a property of a distinct subpopulation of astrocytes?

We have shown previously that the A2B5 monoclonal antibody distinguishes two types of glial fibrillary acidic protein-containing astrocytes in semithin frozen sections of adult rat optic nerve: A2B5- (type-1) astrocytes are found mainly at the periphery of the nerve, where they form the glial limiting membrane, while A2B5+ (type-2) astrocytes are found mainly in the interior of the nerve and constitute more than 65% of the astrocytes in the adult optic nerve. In the present study we show that although most astrocytes in semithin frozen sections of adult rat corpus callosum and optic nerve are A2B5+, the great majority of reactive astrocytes in similar sections of corpus callosum examined 20 weeks after a stab lesion, and in optic nerve examined 20 weeks after adult transection, are A2B5-. Although both A2B5+ and A2B5- astrocytes are stimulated to synthesize DNA in the first week after transection, adult optic nerves examined 20 weeks after transection contain only half as many astrocytes as do normal optic nerves: While A2B5+ astrocytes are reduced almost 10-fold, A2B5- astrocytes are increased by about 25%. We consider the simplest interpretation of these findings to be that type-1 astrocytes are largely responsible for forming glial scars in adult white matter following either a stab lesion or Wallerian degeneration and that in transected optic nerves, most type-2 astrocytes eventually die, possibly because they depend on axons for their long-term survival.