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Single pigeon anterior pituitary glands were incubated with or without a hypothalamus in media containing various drugs. Release of prolactin and growth hormone was quantified by an electrophoretic-densitometric method. The hypothalamus stimulated release of both prolactin and growth hormone from the pituitary gland. Dopamine did not affect hormone release from pituitary glands incubated alone, but inhibited hypothalamus-stimulated release of prolactin and augmented hypothalamus-stimulated release of growth hormone in a dose-related manner. The effects of dopamine were reversed by its antagonist, pimozide. Serotonin stimulated release of prolactin and inhibited release of growth hormone from pituitary–hypothalamus co-incubations, and these effects were blocked by its antagonist, methysergide. Thyrotrophin releasing hormone (TRH) stimulated release of both hormones directly from pituitary glands incubated alone. Dopamine now inhibited TRH-stimulated release of prolactin, without affecting TRH-stimulated release of growth hormone. These results indicate that the neurotransmitters, dopamine and serotonin, affect the in-vitro release of factors from the hypothalamus which control the secretion of prolactin and growth hormone. In addition, dopamine may inhibit release of prolactin directly from the pituitary gland, but only when secretion of prolactin is high initially.
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ABSTRACT
Pituitary glands of grassfrog (Rana pipiens), bullfrog (Rana catesbeiana), clawed toad (Xenopus laevis) and two species of terrapin (Chrysemys picta and Pseudemys scripta) were incubated in medium containing hypothalamic extract (HE), thyrotrophin releasing hormone (TRH), somatostatin, dopamine, or combinations of these treatments. Prolactin and GH concentrations in the medium were determined by densitometry after polyacrylamide-gel electrophoretic separation. Hypothalamic extract stimulated secretion of both hormones in all species tested. Thyrotrophin releasing hormone stimulated secretion of prolactin and GH, showing a biphasic pattern of response. Dopamine had little effect alone, but inhibited HE-and TRH-stimulated release of prolactin, but not GH, in both amphibia and reptiles. Somatostatin by itself had no apparent effect on release of hormones, but it inhibited HE- and TRH-stimulated release of GH from both amphibian and reptilian pituitary glands. These results indicate that factors affecting mammals and birds also interact in the regulation of secretion of prolactin and GH in lower vertebrate species.
J. Endocr. (1984) 102, 175–180
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ABSTRACT
Anterior pituitary glands from broiler fowl were incubated by themselves, with hypothalamic tissue or with thyrotrophin releasing hormone (TRH) in medium containing dopamine and its antagonist pimozide. The presence of hypothalamic tissue or TRH resulted in a stimulation of release of prolactin. Neither dopamine nor pimozide affected prolactin release directly from the pituitary gland. Dopamine inhibited the release of prolactin stimulated by hypothalamic tissue or TRH, in a concentration-dependent fashion. Pimozide diminished the response to dopamine. After pituitary glands were preincubated for 20 h in medium containing oestradiol-17β, the basal release of prolactin was enhanced as was the response to TRH. Both basal and TRH-stimulated release of prolactin from the oestrogen-primed pituitary glands was inhibited by dopamine, an effect blocked by pimozide. Hypothalami from broiler fowl were incubated for up to 8 h in medium containing dopaminergic drugs and pituitary glands were incubated in this medium, alone or with pimozide. As indicated by the prolactin released by the pituitary glands, the hypothalami appeared to secrete prolactin-releasing activity in a time-related fashion. Dopaminergic activity was also present in the hypothalami, since pimozide enhanced the prolactin-releasing activity of the medium. Dopamine apparently inhibited and pimozide stimulated the secretion of releasing activity from the hypothalamus. These results suggest that dopamine inhibits release of prolactin directly from the pituitary gland only when prolactin secretion is high. The hypothalamus secretes at least two factors regulating prolactin secretion, a prolactin-releasing factor and a dopaminergic prolactin-inhibiting factor. Dopamine may also play an inhibitory role in the regulation of secretion of the prolactin-releasing factor.
J. Endocr. (1984) 103, 63–69
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Department of Pure and Applied Zoology, The University, Leeds, LS2 9JT
(Received 17 July 1975)
The tetradecapeptide growth hormone inhibiting factor (GIF), synthesized by Coy, Coy, Arimura & Schally (1973) and Rivier, Brazeau, Vale, Ling, Burgus, Gilon, Yardley & Guillemin (1973), is reported to inhibit growth hormone (GH) secretion in mammals both in vitro and in vivo. It reduces the basal serum GH levels in rats (Brazeau, Rivier, Vale & Guillemin, 1974) and also inhibits the basal release of GH from rat pituitary cells incubated in vitro (Grant, Sarantakis & Yardley, 1974). Growth hormone inhibiting factor abolishes the suckling-induced rise in plasma GH levels in rats (Chen, Mueller & Meites, 1974) and similarly reduces the l-DOPA-stimulated rise in plasma GH in dogs (Lovinger, Boryczka, Shackleford, Kaplan, Ganong & Grumbach, 1974). In man, GIF reduces the serum GH levels artificially raised by means of insulin-induced hypoglycaemia (Schally, Coy, Kastin, Tunbridge, Evered,
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Many cells are able to regulate their sensitivity to hormones. In order to investigate the mechanism(s) by which rat luteal cells regulate their sensitivity to LH, we have developed and characterized a cell culture model. Cultures of dispersed rat luteal cells were exposed to graded doses of bovine LH, an analogue of LH releasing hormone (LH-RH) ([d-Trp6]-LHRH), and prostaglandin F2α (PGF2α) for 3 h. The media containing these hormones were then replaced with fresh hormone-free medium and the cells cultured for 24 h. In order to test the sensitivity of these cultures after 24 h, the medium was discarded and replaced by medium alone, or medium containing a standard dose of bovine LH for 1 h. The amount of cyclic AMP accumulated during this hour was used as an index of the sensitivity of the cells to LH.
Control cultures became 'supersensitive' to LH with augmented production of cyclic AMP during culture but LH-receptor binding activity was not increased. During the first 2 h of culture, LH (100 ng/ml) increased accumulation of cyclic AMP by fourfold, but after 5 h of culture, stimulation of cyclic AMP accumulation by the same dose of LH was increased 32-fold, 299-fold at 13 h and 359-fold at 21 h of culture. The increase in LH-responsive accumulation of cyclic AMP with culture was severely impaired by early exposure of cells to LH, LH-RH analogue or PGF2α during the first 2 h of culture. Also, both LH-RH analogue and PGF2α acutely inhibited LH-stimulated accumulation of cyclic AMP. Inhibition of culture-induced sensitization of LH responsiveness was not altered by the addition of 3-isobutyl-l-methylxanthine. Scatchard analysis of LH binding sites indicated that pretreatment of luteal cells with LH (or human chorionic gonadotrophin at an equivalent dose) reduced the number of free LH receptors when measured after 24 h of culture, but total receptor binding activity was not changed. However, a similar effect was not seen with cells treated with PGF2α or LH-RH analogue.
It is suggested that 'culture-induced' supersensitivity may represent either recovery of preisolation sensitivity or result from the loss of an endogenous factor(s) which retards the coupling of the LH receptor and adenylate cyclase. Although PGF2α and LH-RH analogue have been shown to directly prevent the occupied LH receptor from activation of adenylate cyclase, the present observations have indicated that this inhibitory process was continued even when these agents were removed from the culture medium.
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ABSTRACT
The effects of serotoninergic drugs on adrenocortical function in domestic fowl were examined. Administration of the serotonin receptor agonist 2-(1-piperazinyl)quinoline maleate (quipazine), an inhibitor of serotonin metabolism, N-methyl-N-2-propynylbenzylamine HCl (pargyline), as well as serotonin itself, all increased plasma concentrations of corticosterone. The maximum responses to serotonin and quipazine occurred 1 h after treatment. The quipazine-stimulated response was partly prevented by the serotonin antagonist cyproheptadine. Cockerels pretreated with dexamethasone, a synthetic steroid known to inhibit pituitary ACTH release, showed attenuated responses to subsequent quipazine, pargyline or serotonin injection. Serotonin, quipazine and cyproheptadine did not affect corticosterone release directly from the adrenal gland incubated in vitro, nor did they affect adrenal responsiveness to ACTH stimulation. The neurotoxin 5,6-dihydroxytryptamine injected into day-old chicks decreased plasma concentrations of corticosterone for up to 7 days after treatment, with corresponding decreases in the hypothalamic concentration of serotonin, but not dopamine or noradrenaline concentrations. These results show that adrenal corticosterone secretion is regulated by a central serotoninergic system, probably acting on the hypothalamo-pituitary-adrenal axis.
J. Endocr. (1987) 113,159–165
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ABSTRACT
Calcitonin gene-related peptide (CGRP) and calcitonin are secreted together from medullary thyroid carcinoma (MTC) cells. Interactions of cytosolic free calcium concentration (Cai 2+) and the protein kinase C and A pathways on the secretion of immunoreactive CGRP and calcitonin have been investigated in a human MTC cell line. Ionomycin (10 μmol/l) raised the concentration of Cai 2+, concomitant with a transient stimulation of the secretion of CGRP and calcitonin. 12-O-tetradecanoylphorbol-13-acetate (TPA; 16 nmol/l) did not affect the concentration of Cai 2+, but caused a gradual rise of the secretion of CGRP and calcitonin. Combined addition of 10 μmol ionomycin/1 and 16 nmol TPA/1 resulted in additive stimulation of CGRP and calcitonin secretory responses. Forskolin (10 μmol/l) alone did not change the concentration of Cai 2+, marginally enhanced (P>0·1) the release of CGRP and calcitonin and increased by 23-fold the cellular levels of cyclic AMP (cAMP). Ionomycin and TPA did not change cellular cAMP. Forskolin synergistically enhanced (P<0·01) the ionomycin-induced early phase as well as the TPA-induced late phase of the CGRP and calcitonin secretory responses. In conclusion, increased concentrations of Cai 2+ together with protein kinase C and A activation mediate the secretion of CGRP and calcitonin in MTC cells.
J. Endocr. (1988) 119, 147–152
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ABSTRACT
Pituitary glands and hypothalami from broiler fowl were incubated in medium containing testosterone, and prolactin and GH release were determined. Pituitary glands were also preincubated for 20 h in medium containing testosterone, and then in medium containing various secretagogues.
Testosterone inhibited the release of prolactin directly from the pituitary gland in a concentration-related manner. The hypothalamus stimulated the release of prolactin, but by a lesser amount in the presence of testosterone. When pituitary glands were preincubated with testosterone, subsequent release of prolactin was inhibited, except with the highest concentration which stimulated prolactin release. Hypothalamic extract (HE) markedly stimulated prolactin release from control pituitary glands although testosterone-primed glands were less responsive. The stimulation of prolactin release by thyrotrophin releasing hormone (TRH) and prostaglandin E2 (PGE2) was also reduced by preincubation of the pituitary glands with testosterone.
Priming with testosterone did not affect the release of GH from pituitary glands alone, but reduced the TRH-, HE- and PGE2-stimulated release of GH. These results demonstrate that testosterone directly inhibits prolactin secretion and reduces the sensitivity of pituitary lactotrophs and somatotrophs to provocative stimuli.
J. Endocr. (1984) 102, 153–159
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ABSTRACT
Fowl anterior pituitary glands were bisected and each half was pretreated in either Medium 199 or medium containing EGTA to deplete endogenous calcium (Ca2+) stores, after which they were incubated in Medium 199, or Ca2+-free medium, containing prolactin release-stimulating agents and verapamil, a Ca2+ channel blocker. High K+ concentrations, hypothalamic extract, synthetic thyrotrophin-releasing hormone (TRH) and dibutyryl cyclic AMP (dbcAMP) all stimulated release of prolactin from control (non EGTA-treated) hemianterior pituitary glands. The effects of TRH and dbcAMP were not additive, but the response to submaximal concentrations of TRH was augmented by theophylline, a phosphodiesterase inhibitor. Reduction of Ca2+ availability with EGTA or verapamil reduced basal release of prolactin, prevented the prolactin-stimulating effects of high K+ concentrations and TRH, and markedly attenuated responses to hypothalamic extract and dbcAMP, EGTA being more effective than verapamil. Increasing the Ca2+ concentration of the medium did not augment basal or stimulated release of prolactin.
These results suggest that both Ca2+ and cyclic AMP may act as intracellular mediators in the release of prolactin. Both basal and stimulated release of prolactin depend upon the presence of Ca2+. Although influx from the medium may be the major source of Ca2+, endogenous stores of Ca2+, perhaps mobilized by dbcAMP, may be able to maintain some release of prolactin. The prolactin-stimulating effects of TRH may be mediated by cyclic AMP.
J. Endocr. (1985) 105, 183–188
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ABSTRACT
Immature cockerels were injected with drugs known to affect serotoninergic activity. The receptor agonist quipazine as well as pargyline, an inhibitor of serotonin breakdown, both reduced plasma LH concentrations in a time-dependent fashion. The effect of pargyline was also dose-related. The serotonin precursor, tryptophan, reduced plasma LH levels. Tryptophan and pargyline were as effective in pubertal cockerels as in 3-week-old birds. Responses to quipazine were attenuated by the antagonist, methysergide, although another antagonist, cyproheptadine, also reduced plasma LH levels. Serotonin itself had no effect on plasma LH levels. Parachlorophenylalanine, which blocks serotonin synthesis, had no effect on plasma LH by itself, but attenuated the tryptophan-induced inhibition of LH. These data indicate that serotoninergic mechanisms inhibit secretion of LH in domestic fowl. This mechanism probably operates through the central nervous system.
J. Endocr. (1986) 110, 239–244
