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This Article Full Text Full Text (PDF) All Versions of this Article: 292/1/E203    most recent 00337.2006v1 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 Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Wong, A. O. L. Articles by Lee, E. K. Y. Search for Related Content PubMed PubMed Citation Articles by Wong, A. O. L. Articles by Lee, E. K. Y.

Mechanisms for gonadotropin-releasing hormone potentiation of growth hormone rebound following norepinephrine inhibition in goldfish pituitary cells

Department of Zoology, University of Hong Kong, Hong Kong, China

Submitted 12 July 2006 ; accepted in final form 22 August 2006

In the goldfish, norepinephrine (NE) inhibits growth hormone (GH) secretion through activation of pituitary ₂-adrenergic receptors. Interestingly, a GH rebound is observed after NE withdrawal, which can be markedly enhanced by prior exposure to gonadotropin-releasing hormone (GnRH). Here we examined the mechanisms responsible for GnRH potentiation of this "postinhibition" GH rebound. In goldfish pituitary cells, ₂-adrenergic stimulation suppressed both basal and GnRH-induced GH mRNA expression, suggesting that a rise in GH synthesis induced by GnRH did not contribute to its potentiating effect. Using a column perifusion approach, GnRH given during NE treatment consistently enhanced the GH rebound following NE withdrawal. This potentiating effect was mimicked by activation of PKC and adenylate cyclase (AC) but not by induction of Ca²⁺ entry through voltage-sensitive Ca²⁺ channels (VSCC). Furthermore, GnRH-potentiated GH rebound could be alleviated by inactivation of PKC, removal of extracellular Ca²⁺, blockade of VSCC, and inhibition of Ca²⁺/calmodulin (CaM)-dependent protein kinase II (CaMKII). Inactivation of AC and PKA, however, was not effective in this regard. These results, as a whole, suggest that GnRH potentiation of GH rebound following NE inhibition is mediated by PKC coupled to Ca²⁺ entry through VSCC and subsequent activation of CaMKII. Apparently, the Ca²⁺-dependent cascades are involved in GH secretion during the rebound phase but are not essential for the initiation of GnRH potentiation. Since GnRH has been previously shown to have no effects on cAMP synthesis in goldfish pituitary cells, the involvement of cAMP-dependent mechanisms in GnRH potentiation is rather unlikely.

protein kinase A; protein kinase C; voltage-sensitive Ca²⁺ channel; Ca²⁺/ calmodulin-dependent protein kinase