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Query: UNIPROT:P06889 (Mol)
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Anterior pituitary glands were transplanted beneath the kidney capsule of intact, adult male rats to induce hyperprolactinaemia. This resulted in reduced serum levels of LH and FSH and increased adrenal weight. In pituitary-transplanted rats, testicular hCG-receptor binding was increased by 55 to 175%, whilst the capacity of the testis to secrete testosterone in vitro was greatly reduced. Injection of ovine LH into control and pituitary-transplanted rats resulted in similar percentage reductions in hCG-receptor binding in the two groups. This treatment impaired the in vitro steroidogenic responsiveness of testes from control rats at 24 h after injection, but had no major effect on the already-impaired, steroidogenic responsiveness of testes from pituitary-transplanted rats. Although induction of hyperprolactinaemia resulted in marked changes in Leydig cell function, these alterations were possibly due to the chronically reduced serum gonadotrophin levels in hyperprolactinaemic rats as well as a direct effect of prolactin on the Leydig cell.
Mol Cell Endocrinol 1979 Oct
PMID:The effect of induced hyperprolactinaemia on Leydig cell function and LH-induced loss of LH-receptors in the rat testis. 22 61

Anterior pituitary glands of intact diestrous and gonadectomized female rats were incubated with a supramaximally active dose of LH-RH. Puromycin (P) and cycloheximide (C) did not consistently affect the LH release from glands of ovariectomized rats. In intact rats, LH release induced by LH-RH occurred in two phases, an initial one (relatively slow rate of release) and a secondary one (high rate of release). P and C had no effect on the initial phase, but prevented the secondary one. Pre-incubation with LH-RH prevented the effect of P and C added after 4 hours. Since P and C did not affect the total amount of LH present in media and hypophyses, the LH-released during the P- and C-sensitive phase is not newly formed LH. It is concluded that LH-RH induces the synthesis of protein which is necessary for LH-RH-induced LH release. The initial phase of LH release is made possible by protein already present in the glands at the beginning of the experiment.
Mol Cell Endocrinol
PMID:LH-RH-dependent synthesis of protein necessary for LH release from rat pituitary glands in vitro. 78 57

Anterior pituitary glands from intact dioestrous female rats were incubated in vitro and the LH released into the medium was measured at hourly intervals. The effect of a supramaximally active dose of LH-RH was first inhibited and later augmented by oestradiol added to the medium. The augmented response also occurred when LH-RH was absent during the preceding phase of the incubation. Both effects of oestradiol could be blocked by cycloheximide, which agent, however, also partly inhibited the response to LH-RH.
Mol Cell Endocrinol 1976 Oct
PMID:Inhibitory and augmentative effects of oestradiol on LH-RH-induced release of LH by anterior pituitary glands from intact female rats in vitro. 78 57

Carboxypeptidase H (CP-H) has been characterized in anterior and posterior lobes of bovine pituitary with regard to subcellular distribution, enzymatic properties, nature of membrane association, number of forms and C-terminal processing. Anterior lobe contained both soluble and membrane forms of CP-H with similar enzymatic properties after extraction at pH 5.5. The soluble forms represented about 70% of the total activity. Two soluble and two membrane forms, of 53 and 56 kDa, were demonstrated by immunoblotting and after purification. The amount of the 56 kDa soluble form increased with the salt content of the extraction buffer. Endoglycosidase digestions showed that the difference in size was not due to differential N-linked glycosylation and also showed that CP-H oligosaccharides do not become resistant to endoglycosidase H. CP-H in posterior lobe was also composed from about 70% soluble and 30% membrane forms. Only 53 kDa CP-H was detected in soluble and membrane fractions of posterior lobe. All forms of CP-H from both lobes reacted with antiserum directed to the C-terminus. These results do not support previous observations that soluble and membrane forms of CP-H can be distinguished by size and C-terminal processing.
Mol Cell Endocrinol 1992 Aug
PMID:Carboxypeptidase H in bovine pituitary gland: soluble forms are not processed at the C-terminus. 151 90

It is well established that estrogen modulates central dopamine functions; however, the mechanism of this interaction is still poorly understood. We have used peripheral N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) administration to induce irreversible blockade of dopamine receptors in ovariectomized female rats, which were pretreated with estradiol (10 micrograms, twice each day for 2 weeks) or its vehicle, in order to investigate the effect of estradiol on dopamine receptor repopulation kinetics. As previously observed, chronic estradiol treatment increased both striatal D1 and D2 dopamine receptor densities and left affinities unchanged. Anterior pituitary D2 dopamine receptor density remained unchanged. One day after EEDQ administration, a similar decrease (80%) of [3H]SCH 23390 and [3H]spiperone binding to striatum of estradiol- and vehicle-treated animals was observed. Anterior pituitary D2 dopamine receptor specific binding was reduced by about 50% the day after EEDQ. Recovery after EEDQ administration showed that both receptor production rate and degradation rate constants of anterior pituitary D2 and striatal D1 receptors were slowed after chronic estradiol treatment, whereas recovery rates for striatal D2 dopamine receptors were unaffected. EEDQ administration in vehicle-treated rats did not significantly affect plasma prolactin levels, whereas the combination of estradiol pretreatment and EEDQ administration led to increased plasma prolactin levels, compared with estradiol-treated animals that did not receive EEDQ. This suggests that only a fraction of anterior pituitary dopamine receptors are required for a maximal inhibition of prolactin secretion. Estradiol affected both striatal D1 and D2 dopamine receptor densities but only D1 dopamine receptor repopulation kinetics, suggesting that it may act by different mechanisms on each dopamine receptor. Alternatively, estradiol may affect dopamine receptor interaction. Thus, the present study raises the possibility that a biochemical D1/D2 receptor interaction affects dopamine receptor biosynthesis, turnover, and/or gene expression and that estradiol may influence this dopamine receptor interaction in the striatum.
Mol Pharmacol 1991 May
PMID:Dopamine receptor reappearance after irreversible receptor blockade: effect of chronic estradiol treatment of ovariectomized rats. 167 86

Anterior pituitary glands from individual ovariectomized (ovx) or ovx-estrogen (E2) treated rats were sectioned into 1/8 cubes. Each section was incubated for four consecutive 15 min periods in order to measure the release of immunoreactive and bioactive prolactin (PRL); each individual section was then trypsinized into a single cell suspension for determination of PRL cell numbers in that section. Hormone release (ng PRL/1000 PRL cells) was not uniform throughout the gland; the consistency of the secretory patterns demonstrated that the amount of PRL release from the gland was location-dependent. Statistical analysis of the data showed that the most active cells were in the gland's left lobe, while the least active were in the right lobe. Within these lobes, the dorsal-caudal and ventral-rostral left lobe areas released the most hormone in vitro while those in the dorsal-rostral, dorsal-caudal and ventral-rostral right lobe areas were least active. Injection of ovx rats with E2 for 2 days altered these secretory patterns. This sectioning procedure should prove useful in future studies addressing issues of cell-cell interaction and geographic location as they relate to pituitary cell function.
Mol Cell Endocrinol 1991 Apr
PMID:Function of prolactin cells in the individual rat pituitary gland is location dependent. 182 Sep 75

Follicle-stimulating hormone (FSH)-suppressing protein (FSP) or follistatin, a novel gonadal glycoprotein hormone, has been shown to have chronic inhibitory effects on the secretion of both FSH and luteinizing hormone (LH) in response to gonadotropin-releasing hormone (GnRH) in vitro. The present study was designed to investigate the acute effects of bovine FSP on GnRH-stimulated gonadotropin secretion and to examine the potential subcellular sites of this action of FSP using cultured pituitary cells. Anterior pituitaries from adult male Sprague-Dawley rats were enzymatically dispersed and cultured for 48 h, after which the cells were treated with bovine FSP for 6 h, followed by a 4 h stimulation with secretagogues in the continued presence of FSP. Results showed that the 35 kDa form of bovine FSP (0.1-3 nM) dose-dependently suppressed GnRH-stimulated FSH and LH secretion, with inhibition of 38 and 25%, respectively, at 3 nM. In addition, FSP suppressed gonadotropin secretion in response to activators of protein kinase C (phorbol 12-myristate 13-acetate (PMA) and mezerein) and a calcium ionophore (A23187). However, FSP had no effect on gonadotropin secretion evoked by melittin, an activator of phospholipase A2. Furthermore, 35 kDa bovine FSP did not compete with GnRH for GnRH binding sites in a direct competition study and treatment of cultured pituitary cells with FSP (0.1-3 nM) for 10 h did not alter the number of GnRH binding sites on the cell membranes. Finally, similar inhibitory effects on gonadotropin secretion in response to GnRH, PMA and mezerein were obtained with the 31 and 39 kDa forms of bovine FSP, each at a concentration of 1 nM. We conclude from the present study that FSP acutely inhibits GnRH-stimulated gonadotropin secretion in cultured pituitary cells, and that FSP exerts its action beyond the GnRH receptor, possibly by affecting the protein kinase C and/or the calcium-calmodulin systems.
Mol Cell Endocrinol 1990 Jul 30
PMID:Acute inhibitory effect of follicle-stimulating hormone-suppressing protein (FSP) on gonadotropin-releasing hormone-stimulated gonadotropin secretion in cultured rat anterior pituitary cells. 212 65

The transcriptional regulation of the rat gonadotropin subunit genes was investigated under different regimens of GnRH administration in vitro. Anterior pituitary fragments (8-10/gland) from either intact or ovariectomized CD female rats were treated in static culture with 0.1 or 1 nM GnRH or on perifusion columns with pulsatile GnRH (25 ng pulse every 30 or 60 min) for 1-6 h. Gene transcription rates were measured in nuclear run-off assays, and hemipituitaries from the same animals were matched in control and treatment groups. In static culture, only rates of alpha-subunit mRNA synthesis were stimulated at 1, 3, and 6 h from 64 +/- 10 (control) to 170 +/- 29 (3 or 6 h of GnRH) parts/million (ppm). There was no change in FSH beta mRNA synthesis (28 +/- 6 ppm), and significant stimulation of LH beta was seen only at 1 h (98 +/- 10 vs. 34 +/- 1 ppm for control) with continuous GnRH. Similar results were obtained with both GnRH doses and with pituitaries from either intact or ovariectomized rats. In addition, continuous 1 nM GnRH administration to perifusion columns for 4 or 6 h resulted in no changes in the transcription rate for LH beta (44 +/- 10 vs. 40 +/- 12 ppm for control) or FSH beta (29 +/- 6 vs. 36 +/- 9 ppm for control), but consistent stimulation for alpha-subunit (240 +/- 29 vs. 71 +/- 16 ppm for control). Markedly different results were observed with pulsatile GnRH administration. In perifusion studies, LH beta mRNA synthesis was stimulated 2- to 2.5-fold after 1 h of pulses and 3- to 4-fold after 3 or 6 h. A slight (2-fold) stimulation was noted for FSH beta mRNA synthesis only after 1 h of pulsatile GnRH, while alpha-subunit gene transcription was elevated 2-fold after 1 h and 4- to 5-fold after 3 or 6 h of pulsatile GnRH. GnRH pulses in vivo may also be crucial to maintain gonadotropin mRNA synthesis, since administration of a GnRH antagonist ([Nal-Lys] GnRH; 20 micrograms/100 g BW) suppressed the transcription rate of all three genes to 10-25% of control values after 4 or 24 h. TSH beta mRNA synthesis was not changed by any GnRH treatment, and LH secretion was consistently stimulated by GnRH. No significant differences in transcription rate were noted between GnRH pulse intervals of 30 or 60 min in vitro.(ABSTRACT TRUNCATED AT 400 WORDS)
Mol Endocrinol 1990 Oct
PMID:Effects of gonadotropin-releasing hormone on rat gonadotropin gene transcription in vitro: requirement for pulsatile administration for luteinizing hormone-beta gene stimulation. 212 96

Relaxin is a hormone associated with pregnancy that relaxes uterine smooth muscle and softens the connective tissues of the cervix and pelvis. In spite of these well-characterized tissue responses, the second messenger system linked to the relaxin receptor and the range of target tissues are only modestly understood. We found that relaxin enhanced the cyclic AMP levels in anterior pituitary cells from adult female rats. Relaxin induced a maximal 5.7 +/- 0.5-fold (mean +/- S.E.M.) stimulation of cyclic AMP accumulation and had an excitatory concentration for half-maximal effect (EC50) of 0.4 +/- 0.1 nM, while human relaxin A and B chains had no such activity (EC50 greater than 1 microM). Pertussis toxin amplified the efficacy of relaxin by 1.5 +/- 0.1-fold, indicating the intervention of a G coupling protein. The response to relaxin was reversible with washing, and desensitized slowly with continuous exposure to relaxin. In an attempt to define the physiological role for relaxin at the anterior pituitary, we found that two of the major hypophysiotrophic hormones of the brain (dopamine and somatostatin) markedly inhibited the relaxin stimulation of cyclic AMP. There was also a significant correlation of the response magnitude with the gender of the donor rat. Anterior pituitary cells from adult males exhibited a mean twofold maximal stimulation after relaxin, compared with the sixfold increase measured in cells from female rats. We hypothesize a novel physiological function of relaxin, that of signalling the feminine anterior pituitary.
J Mol Endocrinol 1989 Nov
PMID:Characterization of relaxin-stimulated cyclic AMP in cultured rat anterior pituitary cells: influence of dopamine, somatostatin and gender. 257 41

Pro-vasopressin mRNA, neurophysin and arginine vasopressin (AVP) were assayed in the mouse anterior pituitary gland, in mouse anterior pituitary cells in culture and in the AtT-20 corticotrophic tumour cell line. Northern blot analysis revealed the presence of an approximately 700 base pair pro-vasopressin mRNA in anterior pituitary and AtT-20 cells. Neurophysin, identified by immunoblots, and AVP, identified by high-performance liquid chromatography and cross-reactivity with AVP antiserum, were detected in anterior pituitary cells and AtT-20 cells. Immunocytochemical staining with anti-neurophysin showed that approximately 40-45% of the dissociated anterior pituitary cells in culture and greater than 95% of the AtT-20 cells were stained. Anterior pituitary cells in culture and AtT-20 cells had a basal level of release of AVP in the 0.01-0.1 nM range. These results indicate that anterior pituitary cells and AtT-20 cells have the ability to synthesize and process pro-vasopressin to AVP and neurophysin, endogenously.
J Mol Endocrinol 1988 Jul
PMID:Presence of pro-vasopressin mRNA, neurophysin and arginine vasopressin in mouse anterior pituitary cells and the AtT-20 corticotrophic tumour cell line. 285 8


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