EXPRESSION OF VIMENTIN INCREASES IN THE HIPPOCAMPUS AND CEREBRAL-CORTEX AFTER ENTORHINAL CORTEX LESIONING AND IN RESPONSE TO TRANSFORMING GROWTH-FACTOR-BETA-1

Entorhinal cortex lesions (ECL) that damage the perforant path to the dentate gyrus of the hippocampal formation were used to model the regu lation of vimentin (VIM) mRNA. ECL increased VIM mRNA in the ipsilater al hippocampus and in the ipsilateral cortex including the wound cavit y within 1 day. By in situ hybridization, at 4 days post-ECL, VIM mRNA increased two-fold in the molecular layer of the dentate gyrus. VIM p rotein was co-localized by immunocytochemistry to astrocytes and micro glia/macrophages. Transforming growth factor-beta 1 (TGF-beta 1), whic h was previously shown to increase in microglia/macrophages of the mol ecular layer after hippocampal deafferentation by ECL, was investigate d as a regulator of VIM expression. Infusions of TGF-beta 1 into the l ateral ventricle induced VIM mRNA with dose-dependence, e.g. infusion of 100 ng TGF-beta 1 increased VIM mRNA three-fold. The increase in VI M mRNA was localized by in situ hybridization to astrocytes and microg lia in the molecular layer of the dentate gyrus. These findings furthe r implicate TGF-beta 1 as a regulator of cytoskeletal proteins during synaptic reorganization.