Modulation of γ-actin and α1-tubulin expression by corticosterone during neuronal plasticity in the hippocampus
Abstract Evidence is given for altered gene expression of γ-actin in the hippocampus in response to entorhinal cortex lesion (ECL). Time course analysis reveals a progressive repression of γ-actin expression between 4 and 14 days post-lesion, coinciding with the early and middle phases of the hippocampal reinnervation process. RNA prevalence returns to near control values at 30 days post-lesion. Corticosterone administration, which is known to impair the reinnervation process in ECL rats, prevents the lesion-induced reduction in γ-actin expression and blocks the induction of α1-tubulin in the deafferented hippocampus. The timing of response of γ-actin to ECL and its modulation by glucocorticoid administration support suggestions that γ-actin has an important role to play in neuronal cytoarchitecture remodelling during hippocampal reinnervation.