Abstract
Prolonged over-exposure of rats to corticosterone attenuates 5-HT(1A)-receptor-mediated responses in hippocampal CA1 cells through an unknown mechanism, not involving downregulation of 5-HT(1A) receptor expression. We here tested if corticosterone changes 5-HT(1A) receptor function indirectly, by altering hippocampal mRNA expression of NCAM, SGK1, or RGS4, which all modulate 5-HT(1A) receptor function. We found that the expression of none of these candidates was affected by corticosterone treatment.
MeSH terms
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Animals
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Anti-Inflammatory Agents / pharmacology*
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Corticosterone / pharmacology*
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Hippocampus / drug effects*
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Hippocampus / metabolism
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Immediate-Early Proteins / biosynthesis
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Immediate-Early Proteins / drug effects*
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In Situ Hybridization
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Male
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Neural Cell Adhesion Molecules / biosynthesis
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Neural Cell Adhesion Molecules / drug effects*
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Protein Serine-Threonine Kinases / biosynthesis
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Protein Serine-Threonine Kinases / drug effects*
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RGS Proteins / biosynthesis
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RGS Proteins / drug effects*
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RNA, Messenger / analysis
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Rats
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Rats, Wistar
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Time Factors
Substances
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Anti-Inflammatory Agents
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Immediate-Early Proteins
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Neural Cell Adhesion Molecules
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RGS Proteins
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RNA, Messenger
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RGS4 protein
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Protein Serine-Threonine Kinases
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serum-glucocorticoid regulated kinase
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Corticosterone