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RESEARCH |
Department of Cellular Biology, Physiology and Immunology, University of Córdoba Avda, Menendez Pidal s/n, 14004 Córdoba, Spain and 1 Department of Physiology, University of La Laguna, Spain
Correspondence should be addressed to J E Sánchez-Criado; Email: fi1sacrj{at}uco.es
In the absence of estrogen (E), the selective E receptor modulator tamoxifen (TX) has two agonist effects in the rat pituitary: induction of progesterone receptor (PR)-dependent GnRH self-priming in the gonadotrope, and stimulation of prolactin (PRL) secretion in the lactotrope. TX-induced gonadotropin (GnRH) self-priming is absent when 108 M estradiol-17ß (E2) is added to the incubation medium of pituitaries from TX-treated rats. The present experiments investigated whether PR-independent PRL release into the incubation medium of pituitaries from TX-treated ovariectomized (OVX) rats was affected by E2, and the effect of different ER ligands (ICI182780, TX, estradiol-17
, E2 BSA) on TX-stimulated PRL secretion. Moreover, the effect of E2 on TRH-stimulated PRL secretion in pituitaries collected from estradiol benzoate- and TX-treated OVX rats was studied. It was found that: i) incubation with E2 supressed the PRL releasing effect of injected TX; ii) whereas coincubation with the pure anti-E type II ICI182780 antagonized the inhibitory effect of E2, coincubation with the anti-E type I TX did not; iii) estradiol-17
lacked inhibitory action, whereas a dose-dependent inhibitory effect of both E2 and E2 BSA was noticed; and iv) TRH stimulatory effect on PRL release in pituitaries from TX-treated rats was blocked by addition of E2 to the medium. Taken together, these data argue in favor of the presence of specific membrane recognition sites for E in the lactotrope involved in steroid-specific E2 inhibition of TX-stimulated PRL secretion.
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J. E Sanchez-Criado, J. C Garrido-Gracia, C. Bellido, R. Aguilar, P. Guelmes, P. Abreu, R. Alonso, I. Barranco, Y. Millan, and J. M. de las Mulas Oestradiol-17{beta} inhibits tamoxifen-induced LHRH self-priming blocking hormone-dependent and ligand-independent activation of the gonadotrope progesterone receptor in the rat. J. Endocrinol., July 1, 2006; 190(1): 73 - 84. [Abstract] [Full Text] [PDF] |
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