EXTENSIVE AND LONG-LASTING CHANGES OF GLIAL-CELLS FOLLOWING TRANSECTION OF THE POSTCOMMISSURAL FORNIX IN THE ADULT-RAT

Citation
Cc. Stichel et Hw. Muller, EXTENSIVE AND LONG-LASTING CHANGES OF GLIAL-CELLS FOLLOWING TRANSECTION OF THE POSTCOMMISSURAL FORNIX IN THE ADULT-RAT, Glia, 10(2), 1994, pp. 89-100
Citations number
56
Categorie Soggetti
Neurosciences
Journal title
GliaACNP
ISSN journal
08941491
Volume
10
Issue
2
Year of publication
1994
Pages
89 - 100
Database
ISI
SICI code
0894-1491(1994)10:2<89:EALCOG>2.0.ZU;2-2
Abstract
Injury to the adult brain results in the formation of a glial scar tha t involves both activated astroglia and microglia/macrophages. Althoug h reactive gliosis has been linked to failure of axonal regeneration i n the adult mammalian CNS, the spatio-temporal pattern of the postlesi on responses in morphology and distribution of the major cellular cons tituents of the gliosis has attracted little attention. In an attempt to define these relationships, we have undertaken a systematic study o f astrocytic and microglial/macrophagic responses after stereotactic t ransection of the postcommissural fornix in rat. To visualize astrocyt es, microglia, and macrophages, antibodies against glial fibrillary ac idic protein (GFAP); vimentin (VIM), complement receptor type 3 (OX42) , and ED1 were used. The cellular responses occurring between 2 h and 1 year postlesion (PL) at various distances distal and proximal to the lesion site were studied. Transection of the postcommissural fornix l eads to: 1) a very early microglial reaction both distal and proximal to the lesion, as indicated by OX42-immunoreactivity, followed by a ma ssive astrocytic response; 2) a transient GFAP(-) but VIM(+) region ar ound the lesion center; 3) the appearance of numerous ED1(+) macrophag es at PL3d; and 4) long-lasting (at least 1 year) persistence of both astrocytes and microglia/macrophages. The timing and extension of the sequential glial reactions after postcommissural fornix transection ar e discussed in relation to the myelin degradation and spontaneous spro uting of injured axons that have previously been observed in this lesi on model (Wunderlich et al: Glia 10:49-58, 1994). (C) 1994 Wiley-Liss, Inc.