S-100 is a calcium-binding protein that is predominantly found in astrocytes of the central nervous system. In the present study, we investigated the temporal and spatial changes of S-100beta immunoreactivity after a stereotaxic mechanical lesion of the adult rat corpus callosum performed with an adjustable wire knife. Rats were killed 7, 14 and 28 days after surgery. S-100beta immunoreactivity was found within the cytoplasm and processes of quiescent putative astrocytes that were observed throughout the gray and white matters of the forebrain of sham-operated rats. Following callosotomy, the S-100beta immunoreactive profiles showed increased size and thick processes, as well as increased amount of S-100beta immunoreactivity. Unbiased stereologic analysis revealed a sustained and widespread increase of the Areal Fraction of S-100beta immunoreactive profiles in the medial and lateral regions of the white matter of callosotomized rats at the studied time-intervals. In the cerebral cortex of callosotomized rats, the estimated total number of S-100beta immunoreactive profiles was also increased 7 and 14 days after the lesion. Since the cellular and temporal changes in S-100beta immunoreactivity were closely similar to those described for basic fibroblast growth factor (bFGF) following brain lesions, we co-localized the S-100beta and bFGF immunoreactivities after callosotomy. bFGF immunoreactivity was found in the nuclei of S-100beta immunoreactive glial profiles throughout the forebrain regions of the sham-operated rats. bFGF immunoreactivity was increased in the nuclei of reactive S-100beta immunoreactive putative astrocytes in the forebrain white matter and in the cerebral cortex of callosotomized rats. These results indicate that after transection of the corpus callosum of adult rats, the reactive astrocytes may exert paracrine trophic actions through S-100beta and bFGF. Interactions between S-100beta and bFGF may be relevant to the events related to neuronal maintenance and repair following brain injury.
Copyright 1999 Elsevier Science B.V.