摘要:

The mechanism by which estrogen enhances prolactin (PRL) secretion and induces hyperplasia of lactotrophs is not defined clearly. The objective of this study was to examine hypothalamic monoaminergic PRL regulatory systems and pituitary hormone secretion in the early and later stages of estrogen-induced hyperprolactinemia and pituitary hyperplasia. Dopamine (DA) and serotonin (5-HT) turnover were determined in microdissected brain regions 3 and 30 days after a single subcutaneous dose of estradiol (2 mg) to male ACI rats. Plasma samples were collected in animals with indwelling intra-atrial cannulae. 3 days after estrogen there was a significant increase in plasma PRL, pituitary PRL and growth hormone (GH), and DA turnover in the median eminence and arcuate nucleus. Plasma concentrations and pituitary content of PRL increased at 30 days. The responsiveness of PRL to thyrotropin-releasing hormone (TRH) was enhanced at both times. Concentrations of DA decreased considerably in the median eminence and arcuate nucleus by 30 days, and turnover decreased in the median eminence. 5-HT turnover was not affected in the early stages of hyperprolactinemia. Plasma GH increased and TSH was unchanged, even though pituitary content of both hormones decreased at 30 days. Estrogen had no effect on plasma corticosterone. These findings support the hypothesis that estrogen induces pituitary hyperplasia by antagonizing DA inhibition of PRL-secreting cells and by enhancing their responsiveness to TRH.

ISSN:0028-3835    

DOI:10.1159/000124189

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

In the course of the search for the prolactin-releasing factor (PRF), we noticed that the posterior pituitary contained strong PRF activity and subsequently traced this activity to that of bovine neurophysin-II (NP-II). NP-II prepared in our lab was judged to be a homogeneous preparation according to Sephadex G-75 gel filtration, DEAE ion exchange chromatography and polyacrylamide gel electrophoresis. While neurophysin-I (NP-I) injections of 100 µg/kg and 1,000 µg/kg elevated plasma prolactin in estradiol-primed male rats to 30% and 50% over the control value, respectively, NP-II doses of 100, 1,000 µg/kg increased plasma prolactin concentration in estradiol-primed male rats to 130% and 170% over the control value, respectively. The lowest dose of NP-II needed to increase plasma prolactin concentration was 10 µg/kg. Since neurophysin does not stimulate prolactin release from the ectopic pituitary under the kidney capsule nor from lactotrophs in a primary monolayer culture system, neurophysin is believed to act indirectly on the pituitary, presumably through a neurotransmitter and/or hypothalamic releasing (or inhibiting) factor. We propose that NP-II may be one element in the complex chain of the prolactin-releasing mechan

ISSN:0028-3835    

DOI:10.1159/000124190

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Administration of the serotonin-releasing drug fenfluramine to male rats caused a dose-dependent increase in both plasma prolactin and corticosterone levels. The effect of fenfluramine on prolactin was maximal at 30 min after injection, whereas the effect on plasma corticosterone levels reached a maximum 2 h after injection. In order to determine if the effect of fenfluramine on both hormones was mediated via serotonin release, rats were pretreated with the serotonin uptake inhibitors fluoxetine (10 mg/kg i.p.) or indalpine (10 mg/kg i.p.) 30 min prior to administration of fenfluramine (5 mg/kg i.p.). Both fluoxetine and indalpine inhibited the effect of fenfluramine on plasma prolactin levels, but did not modify the effect of fenfluramine on plasma corticosterone levels. Pretreatment of rats with the serotonin precursor L· tryptophan (100 mg/kg i.p.) potentiated the effect of a submaximal dose of fenfluramine (2 mg/kg i.p.) on plasma prolactin levels, but did not affect the corticosterone response. Depletion of serotonin stores by pretreatment with the serotonin inhibitor p-chlorophenylalanine (300 mg/kg i.p.; 72 h) did not significantly prevent the effect of fenfluramine on either hormone. There was a 34% inhibition of the effect of fenfluramine on plasma prolactin levels, but this effect was not statistically significant. The results of the experiments suggest that the effect of fenfluramine on prolactin secretion is mediated, at least in part, by a serotoninergic mechanism, but the effect on corticosterone secretion is not mediated via serotonin release

ISSN:0028-3835    

DOI:10.1159/000124191

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

In the present study, we have used 125I-cyanopindolol (125ICYP) to identify, characterize, and localize β-adrenergic receptors in bovine, rat, and human pituitary gland by in vitro labeling light microscopic autoradiography. The binding of 125ICYP to slide-mounted bovine pituitary sections was saturable and of high affinity with an apparent Kd of 0.2 nM. The pharmacological profile of 125ICYP binding obtained from competition studies demonstrates that the β-adrenergic receptors in the pituitary gland are predominantly of the β2 subtype. Rat pituitary autoradiograms show specific binding sites for 125ICYP in anterior, intermediate, and posterior lobes with highest concentrations found in the intermediate lobe and progressively lower concentrations in posterior and anterior lobes, respectively. Autoradiograms of 125ICYP binding in human pituitary show a significantly higher concentration of β2-adrenergic receptors in posterior than in anterior lobe of the pituitary. There is a homogeneous distribution of β2-adrenergic receptors within each lobe of both rat and human pituitary glands. The results of the present study provide the first visualization of β2-adrenergic receptors in rat and human pituitary and demonstrate the presence of significant concentrations of β2-adrenergic receptors in the posterior lobe. The data support a role for epinephrine and norepinephrine in modulating pituitary fu

ISSN:0028-3835    

DOI:10.1159/000124192

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

It has been reported that the corticomedial amygdala (CMA) is involved in regulating various hypothalamic and neuroendocrine events. This study examined the role of the CMA in the regulation of the nocturnal surge of prolactin (PRL) induced by cervical stimulation (CS). Female Sprague-Dawley rats were ovariectomized, received CMA or sham lesions, and were placed on a reversed lighting schedule of 14 h light: 10 h dark. 3 weeks later, all rats were cervically stimulated. 5 days after CS (CS + 5) rats were fitted with chronic, intraatrial catheters, and daily progesterone (P) injections (10 mg s.c.) were initiated. On CS + 8, CS + 12, and CS + 15, sequential blood samples were taken from unrestrained rats at 00.00, 02.00, 04.00, 06.00, 08.00, and 10.00 h (animal time). CMA lesions significantly reduced peak PRL levels on CS + 12 and CS+ 15, but not on CS + 8. When ovariectomized CS rats received either 1 or 10 mg P/day and were sampled on CS+ 12, CS+ 15, and CS + 19, CMA lesions reduced the magnitude of the surge on CS+ 12 and CS + 15, a time when P amplification of the surge was apparent. On CS+ 19, when P amplification of the surge was absent, CMA lesions had no effect. CMA lesions greatly reduced peak PRL levels on CS + 12, but not on CS + 8, when rats were lesioned, catheterized, and injected daily with 1 or 10 mg P/day on CS + 3. Similar results were seen in CS rats with their ovaries intact. CMA lesions reduced the magnitude of the nocturnal PRL surge on CS + 12, but not on CS + 8, in pseudopregnant rats that were given 2 mg P/day, in addition to their ovarian P secretion, to extend the occurrence of the surge through CS+ 12. Since lesions of the CMA resulted in blocking the extension of the amplitude of the nocturnal surge, it is suggested that the CMA may play a role in the termination process of the surge. The CMA may mediate at least part of the action of P to delay termination of the surge.

ISSN:0028-3835    

DOI:10.1159/000124193

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The effect of hypo- and hyperthyroidism on the plasma growth hormone (GH) response to synthetic human growth hormone releasing factor (GRF) was determined in conscious, freely moving rats pretreated with chlorpromazine and antiserum against somatostatin. Chlorpromazine plus somatostatin antiserum pretreated rats gave consistent response to GRF which was not observed in untreated rats. Chlorpromazine alone has no effect on GH secretion induced by GRF in rat pituitary monolayer culture. In rats made hypothyroid by thyroidectomy, both basal and peak plasma GH responses to a small (0.25 µg/kg bw) and a moderate dose of GRF (1 µg/kg bw) were significantly reduced as compared to controls. In rats made hyperthyroid by the administration of thyroxine, basal and peak plasma GH responses to a small but not to a moderate dose of GRF were significantly reduced as compared to controls. A reduced plasma GH response to a small dose of GRF was observed 8 days after the cessation of thyroxine administration. The pituitary GH reserve was markedly reduced in hypothyroid but not in hyperthyroid rats as compared to their respective controls. These results indicate that plasma GH response to GRF is reduced both in hypo- and hyperthyroidism. The mechanism involved in the phenomenon appears to be different between the two condition

ISSN:0028-3835    

DOI:10.1159/000124194

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The in vivo internalization of thyrotropin-releasing hormone (TRH) was studied by using a semiquantitative immunoelectron microscopic method. Pituitary glands of normal male rats or of rats intravenously injected with 100 ng TRH and sacrificed after 5–60 min were used. Ultrathin sections were obtained by cryoultramicrotomy of fixed pituitary glands. Pituitary cellular types were identified by appropriate antiserums. An antiserum specifically directed against TRH was used. TRH-like immunoreactivity due to endogenous TRH was observed in thyrotropes and prolactin cells, but never in somatotropes, gonadotropes or corticotropes. At the subcellular level, the reaction was detected within the cytoplasmic matrix, the secretory granules, and the nucleus but only occasionally at the plasma membrane. After in vivo injection of TRH, the immunocytochemical reaction (1) was still restricted to thyrotropes and prolactin cells, (2) increased with time elapsed after injection up to 15–30 min and then returned to basal intensity in cytoplasm, secretory granules, and nucleus, and (3) became very frequent at the plasma membrane. These data (1) provide evidence for endogenous TRH within thyrotropes and prolactin cells, i.e., in physiological target cells for TRH, and (2) support the hypothesis that normal TRH target cells can, in vivo, internalize exogenous as well as endogenous TRH into several subcellular compartments including the nucl

ISSN:0028-3835    

DOI:10.1159/000124195

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Specific lesions of different brain structures known to contain or to be coursed by LHRH neurons have been carried out in intact cycling female rats in order to investigate the role played by central LHRH and neuronal systems in the regulation of ovarian and hypophyseal LHRH receptor (LHRH-R) levels, using the stable LHRH analog [D-Ser (TBU)6] Des-Gly10, LHRH enthylamide, buserelin. Radiofrequency lesions were placed bilaterally or unilaterally into female rats showing at least two consecutive estrous cycles, under pentobarbital anesthesia, while groups of animals were sham-operated. Bilateral lesions placed into the septal area and into the nucleus and tract of the diagonal band of Broca (DBB) resulted in a nearly 25–40% stimulation of LHRH binding activity within the ovaries and a 30% inhibition of LHRH analog binding to pituitary homogenate, while lesions placed into the medial preoptic area (MPO), where the majority of LHRH neurons are found, produced a doubling of ovarian LHRH-R accompanied by a 60% decrease of pituitary binding sites. Lesions involving the median eminence and arcuate hypothalamic nucleus, where the most conspicuous convergence of LHRH fibers occurs, produced a twofold increase in ovarian LHRH-R levels and an almost complete loss of pituitary LHRH-R binding capacity, with no change in affinity. In order to clarify the importance of direct neural signals modulating the ovarian LHRH-R concentration, lesions were placed in the right or left MPO and DBB, and the content of LHRH-R measured in right and left ovaries. Lesions placed unilaterally (right or left) produced a significant increase of LHRH-R binding activity within the ovary ipsilateral to the lesion, while a reduction or no effect was observed in the contralateral gland. Data show a marked stimulation of ovarian LHRH-R number following bilateral lesions placed in the major LHRH-containing structures, while pituitary LHRH binding sites are significantly inhibited, indicating impairment in the rate and/or amplitude of endogenous hypothalamic LHRH release. Furthermore results obtained following unilateral lesions indicate that a neural mechanism is involved in ovarian LHRH receptor induction and further reinforce our view that a direct neural connection links the brain and the ovarie

ISSN:0028-3835    

DOI:10.1159/000124196

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Bilateral intrahypothalamic injections of the brain metabolite quinolinic acid (QUIN) were made in an attempt to examine its effects on the secretion of LH, PRL, GH and TSH. QUIN, a neuroexcitatory amino acid with close structural similarities to glutamate, kainate and N-methylaspartate, was infused into unanesthetized male rats, the animals sacrificed 7.5 min later, and serum hormone concentrations determined by radioimmunoassay. QUIN caused surges in LH, PRL and GH release (316, 607 and 1,134% of control, respectively, at 50 µg QUIN) without affecting the serum concentrations of TSH. At lower doses, a preferential effect of QUIN on PRL release was observed. All QUIN-induced hormonal changes were inhibited by concomitant administration of the specific antagonist ()-2-amino-7-phosphonoheptanoic acid, indicating the presence of QUIN-sensitive receptors on neurons which are intimately associated with endocrine regulation. Moreover, because QUIN-treated animals exhibited behavioral signs of seizure activity and neuroendocrine dysfunction has been reported to occur in human convulsive disorders, the data are also of interest in view of a possible mechanistic link between epileptic phenomena and hormone secretion

ISSN:0028-3835    

DOI:10.1159/000124197

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The neurotransmitter histamine (HA) may participate in the regulation of some pituitary hormones. We, therefore, investigated the effect of HA (50 µg/kg body weight/h, infusion 0–240 min) on basal and thyrotropin-releasing hormone (TRH) and luteinizing hormone releasing hormone (LH-RH) stimulated prolactin (PRL) and LH secretion in 5 normal women during the early follicular and the luteal phases of the same menstrual cycle. HA had no effect on the basal secretion of the two hormones. However, the PRL response to 200 µg TRH during the HA infusion was significantly increased compared to the response to a saline control infusion during the early follicular phase (peak responses were 1,902 ± 398 vs. 1,228 ± 230 µlU/ml, p < 0.025) and during the luteal phase (peak responses were 2,261 ± 335 vs. 1,647 ± 245 µlU/ml, p < 0.05). HA potentiated the LH response to 100 µg LH-RH during the early follicular phase (peak responses were 37.1 ± 4.9 vs. 26.9 ± 4.5 mlU/ml, p < 0.05) and during the luteal phase (peak responses were 79.3 ± 22.5 vs. 50.7 ± 11.4 mlU/ml, p < 0.025). We, therefore, found HA to have a potentiating effect on TRH/LH-RH-stimulated PRL and LH secretion in women. The results are similar to our previous findings in men, although the potentiating effects of HA were h

ISSN:0028-3835    

DOI:10.1159/000124198

出版商:S. Karger AG    

年代:1985

数据来源: Karger