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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adrenalectomy
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Animals
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Corticosterone / pharmacology*
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Cycloheximide / pharmacology
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Hippocampus / drug effects*
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Hippocampus / metabolism
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In Vitro Techniques
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Male
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Membrane Potentials / drug effects
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Microelectrodes
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Mifepristone / pharmacology
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Nerve Tissue Proteins / biosynthesis*
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Neurons / drug effects*
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Neurons / metabolism
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Pyramidal Tracts / cytology
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Pyramidal Tracts / drug effects
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Rats
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Rats, Inbred Strains
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Receptors, Glucocorticoid / drug effects
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Receptors, Glucocorticoid / metabolism
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Receptors, Mineralocorticoid
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Receptors, Steroid / drug effects
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Receptors, Steroid / metabolism
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Serotonin / pharmacology
Substances
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Nerve Tissue Proteins
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Receptors, Glucocorticoid
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Receptors, Mineralocorticoid
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Receptors, Steroid
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Mifepristone
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Serotonin
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Cycloheximide
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Corticosterone