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Long-term control by corticosteroids of the inward rectifier in rat CA1 pyramidal neurons, in vitro.

作者信息

Karst H, Wadman W J, Joëls M

机构信息

Department of Experimental Zoology, University of Amsterdam, The Netherlands.

出版信息

Brain Res. 1993 May 28;612(1-2):172-9. doi: 10.1016/0006-8993(93)91658-f.

DOI:10.1016/0006-8993(93)91658-f
PMID:8330198
Abstract

In this study we examined long-lasting effects mediated by intracellular mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) on two voltage dependent potassium conductances in CA1 pyramidal neurons, i.e. the transient current IA and the delayed rectifier, and on the inward rectifier IQ, a mixed sodium/potassium current. All experiments were carried out in hippocampal slices with the in situ patch clamp technique, in the whole cell mode. Neurons recorded 30 min to 3 h after a brief application of 30 nM corticosterone to slices from adrenalectomized rats, thus saturating MRs and occupying most of the GRs, displayed a large IQ-conductance similar to neurons in slices from the sham-operated controls. By contrast, if only MRs or only GRs were activated, the IQ-conductance was significantly smaller than for the corticosterone-treated group of cells, indicating that simultaneous activation of both MRs and GRs is necessary to achieve a large IQ-conductance. If corticosterone was applied in the presence of a protein synthesis inhibitor, the IQ conductance was significantly smaller than in the absence of the inhibitor. Properties of the IA and the delayed rectifier were not affected by the various corticosteroid treatments. In conclusion, the data indicate that in particular the IQ-conductance is under a gene-mediated control of corticosteroid hormones. The IQ-conductance is relatively low when only MRs are activated, as occurs for the rat in the morning under rest, and high when both MRs and GRs are occupied, as occurs at the peak of the circadian cycle and after stress.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

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引用本文的文献

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Corticosteroids in the brain. Cellular and molecular actions.
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