Literature DB >> 1331681

Modulation of gamma-actin and alpha 1-tubulin expression by corticosterone during neuronal plasticity in the hippocampus.

J Poirier1, D Dea, A Baccichet, S Gauthier.   

Abstract

Evidence is given for altered gene expression of gamma-actin in the hippocampus in response to entorhinal cortex lesion (ECL). Time course analysis reveals a progressive repression of gamma-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 gamma-actin expression and blocks the induction of alpha 1-tubulin in the deafferented hippocampus. The timing of response of gamma-actin to ECL and its modulation by glucocorticoid administration support suggestions that gamma-actin has an important role to play in neuronal cytoarchitecture remodelling during hippocampal reinnervation.

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Year:  1992        PMID: 1331681     DOI: 10.1016/0169-328x(92)90117-t

Source DB:  PubMed          Journal:  Brain Res Mol Brain Res        ISSN: 0169-328X


  2 in total

1.  Beta and gamma actin mRNAs are differentially located within myoblasts.

Authors:  M A Hill; P Gunning
Journal:  J Cell Biol       Date:  1993-08       Impact factor: 10.539

2.  Glucocorticoids regulate protein synthesis in hippocampal slices under mild heat shock conditions.

Authors:  C S Barr; L A Dokas
Journal:  Endocrine       Date:  1998-04       Impact factor: 3.925

  2 in total

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