Copper amplification of prostaglandin E2 stimulation of the release of luteinizing hormone-releasing hormone is a postreceptor event.

Abstract

We have shown that copper amplifies prostaglandin E2 (PGE2) stimulation of luteinizing hormonereleasing hormone (LH-RH) from explants of the median eminence area (MEA) and that this process is calciumdependent. Since a Ca-cAMP pathway has been implicated in PGE2 action on the LH-RH neuron, in this study we wished to ascertain if copper exerts its effect on the PGE2 receptor or on a postreceptor component involved in PGE2 To test these three possibilities, we evaluated the effects of copper on the stimulation of LH-RH release by PGE2 (reaction 1), forskolin (reaction 2), and 8-bromoadenosine 3',5'-cyclic monophosphate (8-bromo-cAMP) (reaction 3), using an in vitro system of median eminence area (MEA) explants. For comparison, we assessed the effect of copper on LH-RH release stimulated by depolarizing concentration of K+, a Ca2+-dependent release process that does not involve an increase in cAMP levels. Our results strongly support the conclusion that copper modulates the functional state of a postreceptor component that is integral to the Ca-cAMP pathway stimulated by PGE2. MATERIALS AND METHODSIn Vitro Incubation. Long Evans male rats (200-250 g) were used. The MEA was dissected (15) 580The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Stimulation of growth by intravenous injection of copper in weanling pigs

“…The impact of high dietary or injected Cu on the growth regulatory system has not been well studied. However, it is known that intravenously injected Cu stimulates the secretion of several neuropeptides in the hypothalamus (Tsou et al, 1977;Barnea and Cho, 1987). Copper was also found to stimulate GH secretion from bovine pituitary explants in vitro (LaBella, 1973).…”

Arachidonic acid, an omega-6 fatty acid, induces cytoplasmic phospholipase A 2 in prostate carcinoma cells

“…It has been proposed that cPLA 2 is activated in response to agents that increase intracellular Ca 2þ , which facilitates translocation of cPLA 2 from the cytosol to the cell membrane, where its substrate is localized (58). AA has been implicated as an ionophore (59) and its product PGE 2 is a known ionophore (60). Since treatment of cells with flurbiprofen reverses the increase in expression caused by endogenous AA (Figure 4), it follows that the increased expression of these genes and enzymes depend upon endogenous synthesis of PGE 2.…”