Abstract
Corticosterone can affect electrical properties of CA1 pyramidal neurons via binding to two corticoid receptor types, the mineralocorticoid (MR) and glucocorticoid receptor (GR). Previously we have shown that MR-activation leads to attenuation of serotonin (5-HT)-induced membrane hyperpolarization, while GR-activation induces an increase in the amplitude of the afterhyperpolarization (AHP) following a short current pulse. In this study we show that the MR- and GR-mediated changes of the membrane properties are prevented in the presence of the protein synthesis inhibitor cycloheximide, thus suggesting a genomic action of the steroids.
Original language | English |
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Pages (from-to) | 27-31 |
Number of pages | 5 |
Journal | Neuroscience Letters |
Volume | 130 |
Issue number | 1 |
DOIs | |
Publication status | Published - 2-Sept-1991 |
Keywords
- CORTICOSTERONE
- MINERALOCORTICOID RECEPTOR
- GLUCOCORTICOID RECEPTOR
- HIPPOCAMPUS
- CA1
- CYCLOHEXIMIDE
- ELECTROPHYSIOLOGY
- RAT-BRAIN
- INVITRO
- GLUCOCORTICOIDS
- MODULATION
- SEROTONIN
- SLICES
- STRESS