Lesion-induced gelsolin upregulation in the hippocampus following entorhinal deafferentation

Gelsolin is an actin-binding protein that regulates actin filament-severing and capping activity in the various processes of cell motilities. Here, we report the expression of gelsolin mRNA and protein in the hippocampus following transections of the entorhinal afferents. Northern blot analysis showed that transcript of gelsolin was upregulated in a transient manner in the cleafferented hippocampus by 1.3-, 2.1-, 1.7-, and 1.1- folds of controls, respectively, at 1, 3, 7, and 15 days postlesion (dpl). In situ hybridization and immunohistochernistry confirmed the temporal expression of gelsolin specifically in the entorhinally denervated zones: the stratum lacunosum-molecular (SLM) of the hippocampus and the outer molecular layer (OML) of the clentate gyrus (DG), which initiated as early as at 1 dpl, reached the maximum at 3 dpl, remained prominently elevated by 7 dpl, and discernibly higher at 15 dpi than that of controls. Double labeling of either gelsolin mRNA or protein with markers of glial cells (Griffonia simplicifolia 104 and CD11b for microglial cells, GFAP for astroglial cells) revealed that gelsolin was highly expressed by both activated microglia and astrocytes. The results suggest that the spatiotemporal upregulation of gelsolin in the hippocampus is induced by entorhinal deafferentation, and that gelsolin would participate in the activation processes of both microglial and astroglial cells and thereby, indirectly play important roles in the subsequent lesion-induced neural reorganization in the hippocampus following entorhinal deafferentation. (c) 2005 Wiley-Liss.