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Laboratory of Cellular Neurobiology, Department of Physiology and
¹ Laboratory of Animal Physiology, Department of Animal Biology, Institute of Biomedical Technologies, University of La Laguna, La Laguna, Spain

(Requests for offprints should be addressed to A Morales; Email: mamoral{at}ull.es)

^* (A Morales and M Gonzalez contributed equally to this work)

The modulatory action of estradiol (E₂) on the GnRH network can be exerted indirectly on presynaptic neurons or directly on estrogen receptors (ERs) located within GnRH hypothalamic neurons. Using the GnRH-producing GT1-7 cell line, we have investigated whether E₂ is able to modify the response of these cells to norepinephrine (NE) stimulation. A 48-h exposure of GT1-7 cells to 10 nM E₂ reduced NE-induced cAMP accumulation. However, 15-min exposure was enough to induce this inhibitory action, provided that a hormone-free period of 48 h after steroid treatment was allowed. Furthermore, this effect was mimicked by E₂ coupled to (E-BSA), indicating that it may be exerted through a membrane-mediated mechanism. In addition, competition experiments using E-BSA coupled to fluorescein isothiocyanate (FITC) revealed the presence of cell membrane-binding sites for E₂. Binding of E-BSA coupled to FITC was blocked by preincubation of cells with either E₂, antiestrogen ICI 182 780, or tamoxifen. Moreover, fluorescence staining of non-permeabilized cells with antibodies against receptors and ß confirmed the presence of both receptor subtypes at the cell membrane. To determine the nature of the ER involved in this response, specific agonists for ER 4,4',4''-(4-propyl-[¹H]pyrazole-1,3,5-triyl)tris-phenol (PPT) and ERß 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) were used. Since PPT, but not DPN, reproduced the effect of E₂, it is suggested that estrogen-induced modulatory action on NE responsiveness was mediated by the ER isoform. Taken together, these results indicate that E₂ modulates the adrenergic sensitivity of GT1-7 cells by a mechanism compatible with the activation of membrane-associated ERs.