A rapid, nongenomic action of glucocorticoids in rat B103 neuroblastoma cells

We report here a new example in which glucocorticoids (GCs) acted in a rapid, nongenomic way. In rat B103 neuroblastoma cells, 5-hydroxytryptamine (5-HT) was found to evoke an immediate rise in intracellular free calcium concentration ([Ca 2+] i). Pre-incubation of B103 cells for 5 min with corticos...

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Bibliographic Details
Published in:Biochimica et biophysica acta 2002-08, Vol.1591 (1), p.21-27
Main Authors: Han, Jian-Zhong, Lin, Wen, Lou, Shu-Jie, Qiu, Jian, Chen, Yi-Zhang
Format: Article
Language:English
Subjects:
5-Hydroxytryptamine
Animals
Calcium
Calcium - metabolism
Drug Interactions
Glucocorticoid
Glucocorticoids - pharmacology
Neuroblastoma - metabolism
Protein kinase C
Rats
Serotonin - pharmacology
Signal Transduction
Tumor Cells, Cultured
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Summary:We report here a new example in which glucocorticoids (GCs) acted in a rapid, nongenomic way. In rat B103 neuroblastoma cells, 5-hydroxytryptamine (5-HT) was found to evoke an immediate rise in intracellular free calcium concentration ([Ca 2+] i). Pre-incubation of B103 cells for 5 min with corticosterone (B) or bovine serum albumin-conjugated corticosterone (B–BSA) concentration-dependently (10 −4–10 −8 M) inhibited the peak increments in [Ca 2+] i. Cortisol and dexamethasone had a similar effect, while deoxycorticosterone and cholesterol were ineffective. This rapid inhibitory effect of corticosterone could be mimicked by protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) and abolished completely by PKC inhibitors Ro31-8220 or GF-109203X. Neither pertussis toxin (PTX) nor nuclear GC receptor (GR) antagonist RU38486 influenced the rapid action of B. Our results suggest that GCs can modulate the 5-HT-induced Ca 2+ response in B103 cells in a membrane-initiated, nongenomic, and PKC-dependent manner.
ISSN:0167-4889
0006-3002
1879-2596
DOI:10.1016/S0167-4889(02)00242-2