Abstract
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 ([Ca2+]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 [Ca2+]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 Ca2+ response in B103 cells in a membrane-initiated, nongenomic, and PKC-dependent manner.
Original language | English (US) |
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Pages (from-to) | 21-27 |
Number of pages | 7 |
Journal | Biochimica et Biophysica Acta - Molecular Cell Research |
Volume | 1591 |
Issue number | 1-3 |
DOIs | |
State | Published - Aug 19 2002 |
Externally published | Yes |
Keywords
- 5-Hydroxytryptamine
- Calcium
- Glucocorticoid
- Protein kinase C
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology