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R. Aguilar, C. Bellido, J. E. Sánchez-Criado and E. Aguilar

Summary. Male rats were grafted on Day 21 of age with 'young' (21 days old) or 'adult' (90 days old) pituitary glands and then treated daily with 4 mg bromocriptine/kg or vehicle. Plasma samples were obtained on Days 21, 25 and 35 and when balano-preputial separation occurred. Both types of grafts advanced the age at which balano-preputial separation occurred and increased prolactin concentrations. Bromocriptine treatment reduced the prolactin values in both grafted groups, but did not block the advancement of puberty in rats treated with 'young' pituitary grafts.

These results suggest the existence of two possible mechanisms in precocious puberty induced by pituitary grafts: one is prolactin-dependent (when 'adult' pituitary glands were used) and the other not directly related to prolactin (when 'young' pituitary glands were used).

Keywords: balano-preputial separation; pituitary graft; prolactin; bromocriptine; testosterone; rat

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C. Bellido, L. Pinilla, R. Aguilar, F. Gaytan and E. Aguilar

Summary. Rats were treated neonatally with oestrogen (500 μg oestradiol benzoate injected on Day 1 of life). Treatment with FSH and LH (80 μg/100 g body wt and 40 μg/100 g body wt respectively) during the early post-natal period (Days 1–10) abolished the effects of oestradiol on the morphological and functional development of the testes and on the regulation of prolactin secretion, but had no action on the effects of oestradiol on the development of the sex accessory glands. Treatment with prolactin (100 μg/100 g body wt) during the early post-natal period did not affect the integrity of the reproductive system in adult life. These results suggest that neonatal oestradiol acts indirectly, through an inhibition of gonadotrophin secretion on testicular development, and directly on the development of the sex accessory glands.

Keywords: neonate; oestrogen; gonadotrophins; testis; sex accessory glands; rat

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L. Pinilla, E. Trimiño, P. Garnelo, C. Bellido, R. Aguilar, F. Gaytán and E. Aguilar

The following experiments were performed: (i) concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and prolactin in plasma were measured at 2, 5, 8, 10 and 15 days in female Wistar rats treated on the first day of life with 100 μg oestradiol benzoate or vehicle; (ii) females injected on day 1 with 100 μg of oestradiol benzoate or 1 mg of testosterone propionate and from day 1 to day 10 or 15 with FSH and LH were killed on day 90; (iii) females injected from day 1 to day 10 or 15 with prolactin or vehicle were killed on day 90; (iv) females injected on day 1 with oestradiol benzoate and from day 1 to day 15 with a luteinizing-hormone-releasing hormone (LHRH) agonist were killed on day 90; (v) groups of females injected on days 1, 4, 7, 10, 13 and 16 with an LHRH antagonist were killed on day 90. Onset of puberty, vaginal cycles, organ weights and hormonal plasma concentrations were measured. Females treated on the first day of life with 100 μg oestradiol showed inhibition of gonadotrophin secretion and stimulation of prolactin secretion during the neonatal period. Females injected on the first day of life with oestradiol benzoate or testosterone propionate showed, in adulthood, anovulation, ovarian atrophy, reduced FSH plasma concentrations, increased prolactin plasma concentrations and reduced pituitary prolactin content. These alterations were due neither to blocked gonadotrophin secretion nor to stimulated prolactin secretion observed immediately after steroid injection, since: (i) development of the anovulatory syndrome was not blocked by the administration of exogenous gonadotrophins or LHRH-agonist; and (ii) blockade of gonadotrophin secretion immediately after birth with an LHRH antagonist or neonatal injection of prolactin did not induce the anovulatory syndrome. It is concluded that anovulation induced by administration of neonatal steroid was mediated neither by the early inhibition of gonadotrophin secretion nor by the stimulation of prolactin secretion.

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R Aguilar, C Bellido, J C Garrido-Gracia, R Alonso and J E Sánchez-Criado

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 10−8 M estradiol-17β (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-17α, 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-17α 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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A Ramírez, L M Hinojosa, J d J Gonzales, D Montante-Montes, B Martínez-Benítez, R Aguilar-Guadarrama, A Gamboa-Domínguez, F Morales, A Carrillo-García, M Lizano, R García-Becerra, L Díaz, A Y Vázquez-Sánchez and J Camacho

Potassium voltage-gated channel, subfamily H (eag-related), member 1 (KCNH1) potassium channels are potential tumour markers and cancer therapeutic targets and are up-regulated by oestrogens and human papilloma virus (HPV) oncogenes. However, the role of KCNH1 in normal tissues is poorly understood, and its expression in pregnancy is unknown. We wondered whether KCNH1 channels are expressed in cervical cells from pregnant patients and whether progesterone (P4) regulates KCNH1. The association with HPV was also investigated. KCNH1 protein expression was studied by immunocytochemistry in liquid-based cervical cytologies; 93 samples were obtained from pregnant patients at different trimesters, and 15 samples were obtained from non-pregnant women (controls). The presence of HPV was studied by PCR with direct sequencing and nested multiplex PCR. HeLa cervical cancer cells were transfected with human progesterone receptor-B (PR-B) and treated with P4. KCNH1 mRNA expression in these cultures was studied by real-time PCR. KCNH1 protein was detected in 100% of the pregnancy samples and in 26% of the controls. We found 18 pregnant patients infected with HPV and detected 14 types of HPV. There was no association between the percentage of cells expressing KCNH1 and either the presence or type of HPV. P4 induced KCNH1 mRNA and protein expression in cells transfected with human PR-B. No regulation of KCNH1 by P4 was observed in non-transfected cells. We show for the first time the expression of an ion channel during human pregnancy at different trimesters and KCNH1 regulation by P4 in human cells. These data raise a new research field for KCNH1 channels in human tissues.