Modifications of Plasma Prolactin Levels and Catecholamine Content in an Ectopic Anterior Pituitary Gland Transplanted under the Kidney Capsule

Fernández-Ruiz, J.J.; Ubeda, E.; Cebeira, M.; Agrasal, C.; Tresguerres, J. A. F.; Ramos, J. A.; Esquifino, Ana I.

doi:10.1159/000180640

Cited by 8 publications

(4 citation statements)

References 13 publications

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“…The mean levels of PRL were significantly higher in SPG recipients than in sham-operated mice (35.7 ± 7.2 vs 6.6 ± 1.8, respectively; mean ± s.e.m., n = 5 in both groups), while GH levels were approximately the same in both groups (26.4 ± 8.2 vs 23.3 + 5.2; mean ± s.e.m.). These results are in good agreement with published data which indicate that PRL is the main product of ectopically transplanted pituitaries (Labrie et al, 1978;Fernandez-Ruiz et al, 1987).…”

supporting

confidence: 93%

Fr-MLV infection induces erythroleukaemia instead of lymphoid leukaemia in mice given pituitary grafts

Fontanini

Basolo²,

Garzelli³

et al. 1990

Br J Cancer

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supporting

confidence: 93%

Fr-MLV infection induces erythroleukaemia instead of lymphoid leukaemia in mice given pituitary grafts

Fontanini

Basolo²,

Garzelli³

et al. 1990

Br J Cancer

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“…Prolactin was measured by RIA using reagents provided by the NI-AMDDK as described previously (28) and the results expressed in terms of NIAMDDK rat prolactin standard RP-3. The sensitivity of the method was 0.020 ngltube and the intrassay coefficient of variation was 3.8%.…”

Section: M Wrwrien T Of Prolac I Inmentioning

confidence: 99%

Effects of Estrogen and Ectopic Pituitary Transplants on the Responsiveness of Pituitary Prolactin Release to Luteinizing Hormone‐Releasing Hormone and Dopamine

Esquifino

Steger

Fernández-Ruiz

et al. 1990

J Neuroendocrinology

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The responsiveness of prolactin release to regulatory inputs depends on the functional state of the lactotrophs. In the present study, we have examined the effects of luteinizing hormone-releasing hormone (LHRH; lo-' or M) on the release of prolactin in vitrofrom hyperplastic pituitaries of estrogen-treated male Fischer rats, ectopic pituitary transplants and in situ pituitaries of grafted and control rats. The effects of dopamine or lo-' M) in this system were also examined. The extent of inhibition of prolactin release by dopamine was not related to the amounts of prolactin secreted under basal conditions or to plasma prolactin levels. LHRH significantly suppressed prolactin secretion in all groups but its effect was most pronounced in the ectopic pituitary transplants and in the hyperplastic pituitaries of animals after chronic exposure to estrogen followed by a period of recovery. Thus, the effects of LHRH on prolactin release appear to be related to the secretory activity andlor to the absolute or relative number of the lactotrophs.Regulation of prolactin secretion from the pituitary involves complex interactions of multiple inhibitory and stimulatory factors (1, 2). The list of factors which can influence prolactin secretion includes luteinizing hormone-releasing hormone (LHRH) but its exact role remains controversial with both stimulatory (3, 4) and inhibitory (5-7) effects having been reported. There is also evidence that the responsiveness of the lactotroph to regulatory influences can be profoundly altered by its prior level of secretory activity and particularly by the prevailing inhibitory inputs (1,8). Therefore, the present study was designed to examine the effects of LHRH on the secretion of prolactin in uitro from the pituitaries in which lactotroph function was chronically stimulated or inhibited in vivo. For these studies hyperplastic, ectopic and in situ pituitaries from rats rendered hyperprolactinemic by chronic estrogen exposure or by multiple ectopic pituitary transplants were used. In order to separate the effects of estrogen itself from the effects of estrogeninduced hyperprolactinemia, we have examined some animals during estrogen treatments and others after the treatment has been discontinued. To more completely assess the functional status and responsiveness of the pituitary tissue, the effects of dopamine on the secretion of prolactin in vitro in the various groups were also compared. ResultsAs expected from previous studies (9-1 l), prolonged exposure of adult male Fischer-344 rats to diethylstilbestrol (DES) resulted in pituitary enlargement and marked elevation of plasma prolactin levels which persisted after removal of DES-containing capsules (Table 1). These effects were more pronounced in the DES-OUT group, almost certainly due to a longer period of exposure to DES (14 vs. 7 weeks). Similarly, transplantation of two or three isologous pituitaries under the renal capsules produced the expected increase in plasma prolactin levels (Table 1).Under basal conditions, pituitar...

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“…The polypeptide hormone prolactin (PRL) is mainly produced and secreted by the pituitary and by the decidua during pregnancy; in addition, an ectopic pituitary graft can increase local PRL levels [ 108 ]. Dopamine plays a major role in regulating the PRL secretion by binding to dopamine D2 receptor (DRD2) in both in-situ and grafted pituitary [ 109 , 110 , 111 ].…”

Section: Resultsmentioning

confidence: 99%

Unveiling the Pathogenesis of Adenomyosis through Animal Models

Wang

Benagiano

Liu

et al. 2022

JCM

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Background: Adenomyosis is a common gynecological disorder traditionally viewed as “elusive”. Several excellent review papers have been published fairly recently on its pathogenesis, and several theories have been proposed. However, the falsifiability, explanatory power, and predictivity of these theories are often overlooked. Since adenomyosis can occur spontaneously in rodents and many other species, the animal models may help us unveil the pathogenesis of adenomyosis. This review critically tallies experimentally induced models published so far, with a particular focus on their relevance to epidemiological findings, their possible mechanisms of action, and their explanatory and predictive power. Methods: PubMed was exhaustively searched using the phrase “adenomyosis and animal model”, “adenomyosis and experimental model”, “adenomyosis and mouse”, and “adenomyosis and rat”, and the resultant papers were retrieved, carefully read, and the resultant information distilled. All the retrieved papers were then reviewed in a narrative manner. Results: Among all published animal models of adenomyosis, the mouse model of adenomyosis induced by endometrial–myometrial interface disruption (EMID) seems to satisfy the requirements of falsifiability and has the predictive capability and also Hill’s causality criteria. Other theories only partially satisfy Hill’s criteria of causality. In particular, animal models of adenomyosis induced by hyperestrogenism, hyperprolactinemia, or long-term exposure to progestogens without much epidemiological documentation and adenomyosis is usually not the exclusive uterine pathology consequent to those induction procedures. Regardless, uterine disruption appears to be a necessary but not sufficient condition for causing adenomyosis. Conclusions: EMID is, however, unlikely the sole cause for adenomyosis. Future studies, including animal studies, are warranted to understand how and why in utero and/or prenatal exposure to elevated levels of estrogen or estrogenic compounds increases the risk of developing adenomyosis in adulthood, to elucidate whether prolactin plays any role in its pathogenesis, and to identify sufficient condition(s) that cause adenomyosis.

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Modifications of Plasma Prolactin Levels and Catecholamine Content in an Ectopic Anterior Pituitary Gland Transplanted under the Kidney Capsule

Cited by 8 publications

References 13 publications

Fr-MLV infection induces erythroleukaemia instead of lymphoid leukaemia in mice given pituitary grafts

Fr-MLV infection induces erythroleukaemia instead of lymphoid leukaemia in mice given pituitary grafts

Effects of Estrogen and Ectopic Pituitary Transplants on the Responsiveness of Pituitary Prolactin Release to Luteinizing Hormone‐Releasing Hormone and Dopamine

Unveiling the Pathogenesis of Adenomyosis through Animal Models

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