Corticosterone-induced responses in rat brain RNA are also evoked in hippocampus by acute vibratory stress.

Corticosterone (CORT) induces responses in brain cells that are mediated by glucocorticoid receptors through regulation of gene activity. We previously found rapid increases in select poly(A)-containing RNAs in rat hippocampus following treatment with CORT that are mediated by low-affinity glucocorticoid receptors. To determine if these responses are hippocampal specific, we examined RNA responses to glucocorticoids in several brain regions, myocardium, and cultured astrocytes by two-dimensional gel electrophoretic resolution of 35S-methionine labelled, in vitro translation products. RNAs coding for similar 35-, 33-, and 20-kdalton polypeptides are induced after 3 days of CORT treatment (40 mg/kg/day) in hippocampus, hypothalamus, cortex, striatum, cerebellum, and myocardium. Primary astrocyte cultures (neonatal rat), however, showed increases after hydrocortisone (1 microgram/ml) in only the 20- and 33-kdalton translation products, while the 35-kdalton polypeptide was not detected. The hippocampal responses were maintained for up to 3 months during chronic daily CORT treatment. To determine if an increase in endogenous CORT levels would also evoke the RNA responses, we subjected rats to 2 h vibratory stress and analyzed the in vitro translation products. RNAs coding for the 35- and 20-kdalton polypeptides were increased 3- to 5-fold in the hippocampus after acute stress in intact rats, but not in stressed adrenalectomized rats. These results suggest a new class of molecular stress responses in brain cells that is glucocorticoid dependent under physiological conditions.