Permissive and non‐permissive reactive astrocytes: Immunofluorescence study with antibodies to the glial hyaluronate‐binding protein

Abstract

Two distinct types of reactive astrocytes were studied in rat CNS. Reactive astrocytes secondary to penetrating trauma (anisomorphic gliosis) were induced by stab wounds to the brain. Reactive astrocytes secondary to Wallerian degeneration (isomorphic gliosis) were induced in spinal cord dorsal columns by dorsal rhizotomy proximal to dorsal root ganglia. Anisomorphic glial scars did not stain with antibodies to the glial hyaluronate-binding protein (GHAP), a structural glycoprotein of white matter extracellular matrix. Conversely, isomorphic glial scars were still GHAP-positive 3 months after dorsal root transection. Only after 5 months did GHAP immunoreactivity start to disappear from the isomorphic glial scar. Extensive dorsal rhizotomy was performed at the lumbar level to produce Wallerian degeneration of spinal cord dorsal columns. One month later, the rats were reoperated and two thoracic dorsal roots were implanted in the degenerated dorsal columns. The rats were examined 1 month after grafting. As expected, there was a dense anisomorphic glial scar at the site of surgery, while the dorsal columns above the graft showed isomorphic gliosis. Extensive axonal growth was observed in the dense glial scar surrounding the graft. Conversely, no axonal growth was observed in the degenerated dorsal columns undergoing isomorphic gliosis above the implant. The findings suggested that GHAP-negative astrocytes responding to traumatic injury are permissive for axonal growth and that GHAP-positive astrocytes responding to Wallerian degeneration are not permissive.

Vascular and Glial Changes in the Retrolaminar Optic Nerve in Glaucomatous Monkey Eyes

“…The cellular reactions occurring in glaucomatous optic nerve atrophy were similar to those described for optic nerves undergoing Wallerian degeneration: staining for GFAP [22]and vimentin increases [23, 24], while the total number of astrocytes remains constant [32]. Accumulation of GFAP and vimentin also occurs in white matter astrocytes after axonal injury [33, 34]. In human open-angle glaucoma, changes in the extracellular material and in immunohistochemical staining of astrocytes for GFAP and neural cell adhesion molecule have been described [35, 36].…”

Robust Regeneration of Adult Sensory Axons in Degenerating White Matter of the Adult Rat Spinal Cord

“…Survival 8 d after transplantation. Scale bars, 250 m. (Mansour et al, 1990;Hoke and Silver, 1994), and that proximity to the immediate vicinity of a lesion determines whether the reactive glial environment will be growth-supportive or inhibitory. We were most excited to learn that even after relatively long periods (3 months), the distal tract still remained permissive for the regeneration of sensory axons, although there were indications that white matter nearer the pial surface within 3 mm of the lesion was becoming refractory to axon growth.…”

Can mammalian vision be restored following optic nerve degeneration?

“…37 Within the CNS, activated astrocytes form a dense plug of gliotic tissue in an attempt to wall off the CNS from pathogens and reestablish the blood-brain barrier. 38 Thus, gliosis inhibits axon regeneration directly by presenting a physical barrier to regrowing axons and indirectly by the synthesis of regeneration-inhibiting molecules. 39 …”