NDLI: Regulation of CaV3.1 Channels by Glucocorticoids

Content Provider	Springer Nature Link
Author	Avila, Traudy Hernández Hernández, Oscar Almanza, Angélica Bermúdez de León, Mario Urban, Mercedes Soto, Enrique Cisneros, Bulmaro Felix, Ricardo
Copyright Year	2009
Abstract	The activity of low voltage-activated Ca2+ (CaV3) channels is tightly coupled to neurotransmitter and hormone secretion. Previous studies have shown that CaV3 channels are regulated by glucocorticoids (GCs), though the mechanism underlying channel regulation remains unclear. Here, using the pituitary GH3 cell line as a model, we investigated whether CaV3 channel expression is under the control of GCs, and if their actions are mediated by transcriptional and/or post-transcriptional mechanisms. RT-PCR and western blot analyses showed that CaV3.1 but not CaV3.2 and CaV3.3 channels is expressed in the GH3 cells, and patch clamp recordings confirmed that Ca2+ currents through low voltage-activated channels were decreased after chronic treatment with GCs. Consistent with this, total plasma membrane expression of CaV3.1 protein as analyzed by cell-surface biotinylation assays and semi-quantitative western blotting was also down-regulated, while quantitative real-time RT-PCR analysis revealed a significant decrease of CaV3.1 mRNA expression in the treated cells. In contrast, patch-clamp recordings on HEK-293 cells stably expressing recombinant CaV3.1 channels showed that Ca2+ currents were not affected by GC treatment. These results suggest that decreased transcription is a likely mechanism to explain the inhibitory actions of GCs on the functional expression of native CaV3.1 channels.
Starting Page	1265
Ending Page	1273
Page Count	9
File Format	PDF
ISSN	02724340
Journal	Cellular and Molecular Neurobiology
Volume Number	29
Issue Number	8
e-ISSN	15736830
Language	English
Publisher	Springer US
Publisher Date	2009-06-16
Publisher Place	Boston
Access Restriction	Subscribed
Subject Keyword	Ca2+ channels CaV3.1 Cortisol Dexamethasone GH3 cells HEK-293 cells Animal Anatomy / Morphology / Histology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Cellular and Molecular Neuroscience

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