Hippocampal microglial activation associated with facial nerve injury

Introduction. Facial nerve injury induces changes on hippocampal long-term synaptic plasticity and affects object recognition memory and spatial memory consolidation, both hippocampal-dependent tasks. Although microglial activation has been described in the primary motor cortex associated with this type of lesion, it is not known if something similar occurs in the hippocampus. The existence of microglial changes in hippocampal tissue, associated with this peripheral nerve injury, could explain the previously described neuronal changes in this brain structure. Objective. Characterize the effect of the unilateral facial nerve injury on microglial proliferation and activation in contralateral hippocampus. Materials and methods. Immunohistochemical experiments were done to detect microglial cells in hippocampal tissue of rats with facial nerve lesion. The animals were sacrificed at different times after the injury to evaluate the evolution of proliferation (cell's density) and activation (cell ' s area) of hippocampal microglial cells. Sham-operated animals were compared with lesioned animals sacrificed at 1, 3, 7, 21 or 35 days after injury. Results. The hippocampal microglial cells of facial nerve injured animals showed proliferation and activated phenotype between 3- and 21-days post-lesion. These modifications are transient, since the microglial cells return to the resting state five weeks after injury, despite the irreversible nature of the lesion. Conclusions. Facial nerve injury causes transient proliferation and activation of microglial cells in the hippocampus. This finding could be involved in the generation of morphological and electrophysiological changes described in CA1 pyramidal neurons and in the impairments of spatial memory consolidation, previously observed in facial nerve injured animals.