摘要
We have examined acute effects of corticosterone (CORT) on N-methyl-D-aspartate (NMDA) receptor-mediated Ca2+ signals in adult mouse hippocampal slices. We found so far that the 30 min preincubation of CORT induced a signifcant decrease of the peak amplitude of NMDA-induced Ca2+ elevation in the CA1 region. The membrane non-permeable bovine serum albumin-conjugated CORT also induced a similar effect in the CA1 region. Therefore the acute CORT effects should be induced via putative surface CORT receptors. A possible candidate is a classical intracellular glucocorticoid receptor (GR). To confirm this speculation, we here examined the effects of dexamethasone (DEX: an agonist of GR) and CORT with RU38486 (an antagonist of GR) on NMDA-induced Ca2+ signals. As a result, DEX induced a similar effect to the suppressive CORT effect in the CA1 region, and RU38486 inhibited the suppressive CORT effect. These results indicate that the surface CORT receptor should be GR bound to plasma mem- brane.
We have examined acute effects of corticosterone (CORT) on N-methyl-D-aspartate (NMDA) receptor-mediated Ca2+ signals in adult mouse hippocampal slices. We found so far that the 30 min preincubation of CORT induced a signifcant decrease of the peak amplitude of NMDA-induced Ca2+ elevation in the CA1 region. The membrane non-permeable bovine serum albumin-conjugated CORT also induced a similar effect in the CA1 region. Therefore the acute CORT effects should be induced via putative surface CORT receptors. A possible candidate is a classical intracellular glucocorticoid receptor (GR). To confirm this speculation, we here examined the effects of dexamethasone (DEX: an agonist of GR) and CORT with RU38486 (an antagonist of GR) on NMDA-induced Ca2+ signals. As a result, DEX induced a similar effect to the suppressive CORT effect in the CA1 region, and RU38486 inhibited the suppressive CORT effect. These results indicate that the surface CORT receptor should be GR bound to plasma mem- brane.
