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This Article Full Text Full Text (PDF) All Versions of this Article: 286/4/E626    most recent 00088.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Hyde, G. N. Articles by Borski, R. J. Search for Related Content PubMed PubMed Citation Articles by Hyde, G. N. Articles by Borski, R. J.

Cortisol rapidly suppresses intracellular calcium and voltage-gated calcium channel activity in prolactin cells of the tilapia (Oreochromis mossambicus)

¹Department of Zoology, North Carolina State University, Raleigh, North Carolina 27695; and ²Department of Zoology and Hawaii Institute of Marine Biology, University of Hawaii, Kaneohe, Hawaii 96744

Submitted 26 February 2003 ; accepted in final form 19 November 2003

Cortisol was previously shown to rapidly (10-20 min) reduce the release of prolactin (PRL) from pituitary glands of tilapia (Oreochromis mossambicus). This inhibition of PRL release by cortisol is accompanied by rapid reductions in ⁴⁵Ca²⁺ and cAMP accumulation. Cortisol's early actions occur through a protein synthesis-independent pathway and are mimicked by a membrane-impermeable analog. The signaling pathway that mediates rapid, nongenomic membrane effects of glucocorticoids is poorly understood. Using the advantageous characteristics of the teleost pituitary gland from which a nearly pure population of PRL cells can be isolated and incubated in defined medium, we examined whether cortisol rapidly reduces intracellular free calcium () and suppresses L-type voltage-gated ion channel activity in events that lead to reduced PRL release. Microspectrofluorometry, used in combination with the Ca²⁺-sensitive dye fura 2 revealed that cortisol reversibly reduces basal and hyposmotically induced within seconds (P < 0.001) in dispersed pituitary cells. Somatostatin, a peptide known to inhibit PRL release through a membrane receptor-coupled mechanism, similarly reduces . Under depolarizing [K⁺], the L-type calcium channel agonist BAY K 8644, a factor known to delay the closing of L-type Ca²⁺ channels, stimulates PRL release in a concentration-dependent fashion (P < 0.01). Cortisol (and somatostatin) blocks BAY K 8644-induced PRL release (P < 0.01; 30 min), well within the time course over which its actions occur, independent of protein synthesis and at the level of the plasma membrane. Results indicate that cortisol inhibits tilapia PRL release through rapid reductions in that likely involve an attenuation of Ca²⁺ entry through L-type voltage-gated Ca²⁺ channels. These results provide further evidence that glucocorticoids rapidly modulate hormone secretion via a membrane-associated mechanism similar to that observed with the fast effects of peptides and neurotransmitters.

BAY K 8644; nongenomic actions; glucocorticoids; osmoregulation; nifedipine; L-type voltage-gated ion channels; teleost