Entorhinal deafferentation induces the expression of profilin mRNA in the reactive microglial cells in the hippocampus.

Abstract

Profilin has been identified as an actin monomer sequestering protein and is thought to be a key regulator of actin polymerization in many fundamental cellular processes. We report the expression of profilin mRNA in the murine hippocampus following transections of the entorhinal afferents. Northern blot analysis showed that transcript of profilin was upregulated in a transient manner in the deafferented rat hippocampus by 1.5-, 1.9-, 1.4-, and 1.1-fold of controls, respectively, at 1, 3, 7, and 15 days post-lesion. In situ hybridization confirmed the temporal upregulation of profilin mRNA in the deafferented zones of the mouse hippocampus, which showed a remarkable increase as early as at 1 day post-lesion, reached maximal level at 3 days post-lesion, and returned to the control level at 15 days post-lesion. The expression modulation of profilin mRNA was observed to occur specifically in the entorhinally denervated zones: the stratum lacunosum-moleculare of the hippocampus and the outer molecular layer of the dentate gyrus. The combination of in situ hybridization for profilin mRNA with lectin cytochemistry for Griffonia simplicifolia IB4 showed that the cells expressing profilin transcript in the denervated zones are activated microglial cells. The results suggest that the spatial and temporal upregulation of profilin mRNA in the hippocampus is induced by entorhinal deafferentation and profilin is involved in microglial activation associated with morphological change, migration, and phagocytic behavior of microglial cells.