| Autor: |
W. A. Arden, Paul G. Wagner, Brian A. Jackson, Mark S. Jorgensen |
| Rok vydání: |
1999 |
| Předmět: |
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| Zdroj: |
Journal of Neuroscience Research. 57:643-650 |
| ISSN: |
0360-4012 |
| DOI: |
10.1002/(sici)1097-4547(19990901)57:5<643::aid-jnr6>3.0.co;2-e |
| Popis: |
Recent studies from this laboratory have established that long-term exposure (48 hr) to glucocorticoids can modulate voltage-gated Ca(2+) channel activity and subsequent intracellular Ca(2+) transients in porcine adrenal medullary chromaffin (PAMC) cells maintained in primary culture. Consistent with many steroid hormone-mediated responses, this chronic effect of glucocorticoids probably involves increased gene expression and protein synthesis. However, there is now considerable evidence to suggest that steroids can also elicit acute, non-genomic effects. The aim of the present study was to determine whether acute exposure to glucocorticoids also affects nicotinic receptor-dependent catecholamine (CAT) secretion and Ca(2+) signaling in PAMC cells. Acute exposure to dexamethasone (DEX) dose-dependently attenuated the degree of nicotine (NIC)-induced CAT secretion, as well as the amplitude of NIC-induced intracellular Ca(2+) transients. Significant inhibition of CAT secretion occurred immediately upon addition of DEX, reached maximal levels within 5 min of exposure to DEX, and was rapidly reversible after steroid washout. The endogenous porcine glucocorticoid cortisol elicited similar effects. In contrast, DEX had no significant effect on KCl-induced CAT secretion or intracellular Ca(2+) transients. These data demonstrate that acute exposure to glucocorticoids can modulate stimulus-secretion coupling in PAMC cells and suggest that the primary site of action is the nicotinic receptor. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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