RESUMEN
BACKGROUND: The prostate is a key gland in the sexual physiology of male mammals. Its sensitivity to steroid hormones is widely known, but its response to prolactin is still poorly known. Previous studies have shown a correlation between sexual behaviour, prolactin release and prostate physiology. Thus, here we used the sexual behaviour of male rats as a model for studying this correlation. Hence, we developed experimental paradigms to determine the influence of prolactin on sexual behaviour and prostate organization of male rats. METHODS: In addition to sexual behaviour recordings, we developed the ELISA procedure to quantify the serum level of prolactin, and the hematoxilin-eosin technique for analysis of the histological organization of the prostate. Also, different experimental manipulations were carried out; they included pituitary grafts, and haloperidol and ovine prolactin treatments. Data were analyzed with a One way ANOVA followed by post hoc Dunnet test if required. RESULTS: Data showed that male prolactin has a basal level with two peaks at the light-dark-light transitions. Consecutive ejaculations increased serum prolactin after the first ejaculation, which reached the highest level after the second, and started to decrease after the third ejaculation. These normal levels of prolactin did not induce any change at the prostate tissue. However, treatments for constant elevations of serum prolactin decreased sexual potency and increased the weight of the gland, the alveoli area and the epithelial cell height. Treatments for transient elevation of serum prolactin did not affect the sexual behaviour of males, but triggered these significant effects mainly at the ventral prostate. CONCLUSION: The prostate is a sexual gland that responds to prolactin. Mating-induced prolactin release is required during sexual encounters to activate the epithelial cells in the gland. Here we saw a precise mechanism controlling the release of prolactin during ejaculations that avoid the detrimental effects produced by constant levels. However, we showed that minor elevations of prolactin which do not affect the sexual behaviour of males, produced significant changes at the prostate epithelium that could account for triggering the development of hyperplasia or cancer. Thus, it is suggested that minute elevations of serum prolactin in healthy subjects are at the etiology of prostate abnormal growth.
Asunto(s)
Prolactina/fisiología , Próstata/fisiología , Conducta Sexual Animal/fisiología , Animales , Ritmo Circadiano , Eyaculación/fisiología , Células Epiteliales/fisiología , Haloperidol/farmacología , Inyecciones Subcutáneas , Masculino , Concentración Osmolar , Adenohipófisis/trasplante , Prolactina/sangre , Prolactina/metabolismo , Prolactina/farmacología , Próstata/efectos de los fármacos , Próstata/metabolismo , Próstata/patología , Ratas , Ratas WistarRESUMEN
This study was designed to investigate the effect of hyperprolactinemia, with high or low estrogen levels, on the response to imipramine in the forced swimming test. Three groups of female rats were studied: (1) ovariectomized controls, with low serum prolactin (PRL) and estrogen levels, (2) ovariectomized, estrogen-treated rats, with high PRL and high estrogen levels, and (3) pituitary-grafted rats, with high PRL and low estrogen levels. The hyperprolactinemic groups did not show significant behavioral changes in the forced swimming test preceded by saline injection. Imipramine decreased the immobility time by 37.5% in ovariectomized controls but not in the pituitary-grafted group, and there was an increment of 48.4% in immobility time following imipramine administration in the estrogen-treated group (p<0.05). This paradoxical response to imipramine was significantly correlated with serum PRL (r = 0.59, p<0.01) but not with estradiol levels. These findings suggest that, at least in female rats submitted to the forced swimming model, PRL may induce reversed behavioral effects in response to imipramine, independently of circulating estrogen levels.
Asunto(s)
Hiperprolactinemia/fisiopatología , Imipramina/farmacología , Natación/fisiología , Animales , Conducta Animal/efectos de los fármacos , Conducta Animal/fisiología , Estradiol , Femenino , Hiperprolactinemia/inducido químicamente , Locomoción/efectos de los fármacos , Locomoción/fisiología , Ovariectomía , Adenohipófisis/metabolismo , Adenohipófisis/trasplante , Prolactina/sangre , Ratas , Ratas Wistar , Tiempo de Reacción/efectos de los fármacos , Tiempo de Reacción/fisiologíaRESUMEN
The release of prolactin (PRL) and growth hormone (GH) of pituitary grafts and in situ glands was investigated using perifusion techniques. Whole pituitary or anterior lobe grafts were used. The grafts or the in situ glands were incubated alone in a chamber. The hypophysis of dioestrous-1 glands were used as controls. Both types of grafts released PRL an GH to the medium, being the PRL release of the anterior lobe graft higher than that of the whole pituitary graft. The in situ pituitary glands of grafted animals released less PRL than the control dioestrous glands. Also, the in situ glands of whole pituitary grafted animals released less PRL than the hypophysis of animals which bore grafts of only the anterior lobe. No difference in GH secretion, either by the graft or by the in situ gland was observed when whole pituitary or anterior grafts were used. These results provide a further support to the hypothesis that a pituitary graft under the kidney capsule exerts profound modifications in the function of the in situ hypophysis. The presence of the neurointermediate lobe (NIL) in the graft is modulatory to the release of PRL.
Asunto(s)
Hormona del Crecimiento/metabolismo , Hipófisis/metabolismo , Prolactina/metabolismo , Animales , Femenino , Hipófisis/fisiología , Hipófisis/trasplante , Adenohipófisis/metabolismo , Adenohipófisis/fisiología , Adenohipófisis/trasplante , Radioinmunoensayo , Ratas , Ratas EndogámicasRESUMEN
Substance P, an undecapeptide isolated from gut and brain tissues, was reported to stimulate prolactin release. It was suggested that substance P may play a role in the control of prolactin secretion. In this investigation we studied the effects of the blockade of endogenous substance P by the administration of a specific anti-substance P serum on serum prolactin levels in rats in the evening of proestrus, in lactating rats after suckling, and in male rats with hyperprolactinemia induced by grafting 2 anterior pituitary glands under the kidney capsule. The injection of the anti-substance P serum was followed by a significant decrease of the prolactin surge induced by 30 min suckling in lactating rats, when the antiserum was administered 24 hr but not 5.30 hr earlier. Anti-substance P serum also induced a significant decrease in serum prolactin levels in pituitary grafted rats, but induced no change in the proestrous surge of prolactin and LH. These results show that substance P may be involved in the release of prolactin induced by suckling and that this peptide may have an intrapituitary role in the process of prolactin release. On the other hand, substance P does not seem to play a significant role in the proestrous peak of prolactin and LH.