Modulation of gamma-actin and alpha 1-tubulin expression by corticosterone during neuronal plasticity in the hippocampus.
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.
Poirier
J
J
Douglas Hospital Research Centre, Verdun, Que, Canada.
Dea
D
D
Baccichet
A
A
Gauthier
S
S
D000199:Actins / Q000096:biosynthesis*; D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D015152:Blotting, Northern; D003345:Corticosterone / Q000494:pharmacology; D003714:Denervation; D005786:Gene Expression Regulation / Q000502:physiology*; D005815:Genetic Code / Q000235:genetics; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism*; D007091:Image Processing, Computer-Assisted; D008297:Male; D009473:Neuronal Plasticity / Q000502:physiology*; D051381:Rats; D011916:Rats, Inbred F344; D014404:Tubulin / Q000096:biosynthesis*
D000199:Actins; D014404:Tubulin; D003345:Corticosterone