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SUMMARY
Various agents were tested for their ability to oppose the stimulatory effect of dibutyryl cyclic AMP on the release of the melanocyte-stimulating hormone from the rat neuro-intermediate lobe in vitro. Only dopamine exhibited an inhibitory effect; serotonin, γ-aminobutyric acid, tocinoic acid, tocinamide, the tripeptide Pro-Leu-Gly-NH2 and dibutyryl cyclic GMP were all ineffective.
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Increase of plasma prolactin in chronically ovariectomized rats by transplanting pituitary glands from male rats to the kidney capsule reduced pituitary LH output for 1 week. At the end of this time, despite the fact that prolactin remained high, plasma LH levels rose to reach the value seen in ovariectomized control rats. High plasma prolactin did not affect FSH concentrations. Treatment of ovariectomized rats with apomorphine, a dopamine-receptor stimulating drug, reduced pituitary LH release in a dose-dependent way at doses of 1, 2, 5 and 10 mg/kg body weight. Higher doses either had no effect or they stimulated pituitary LH release. Apomorphine did not reduce pituitary LH secretion in chronically hyperprolactinaemic rats at doses which significantly inhibited LH release in ovariectomized animals. Plasma FSH levels were not affected by apomorphine treatment. In both groups of animals the drug reduced plasma prolactin levels to basal values, indicating that the dopamine agonist inhibits pituitary prolactin release by direct action on the pituitary gland.
These results suggest that dopamine inhibits pituitary LH release, probably by reducing hypothalamic LH-releasing hormone release. The mechanism by which chronically high prolactin levels cause apomorphine to be less effective in reducing pituitary LH release may be a desensitization of some dopamine-receptive mechanism which is inhibitory to LH release.
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ABSTRACT
Patterns of prolactin release were examined using stimulating and inhibiting agents. Primary cultured pituitary cells primed with oestrogens were used for perifusion experiments. TRH (100 nmol/l) increased the peak prolactin concentration to 360% of the basal concentration, while TRH, under inhibition by 1 nmol somatostatin/l, raised the peak prolactin concentration to 185% of the basal levels. When the somatostatin concentration was increased to 10, 100 and 1000 nmol/l, TRH still stimulated prolactin release to 128%, 121% and 140% respectively, indicating that concentrations of somatostatin of 10 nmol/l or higher did not further suppress the stimulatory effect of TRH. TRH (1 μmol/l) stimulated prolactin release under the influence of 0 (control), 1, 10, 100 and 1000 nmol dopamine/l (plus 0·1 mmol ascorbic acid/l) to 394, 394, 241, 73 and 68% of the basal concentration respectively, showing that the dopamine concentrations and peak prolactin concentrations induced by TRH have an inverse linear relationship in the range 1–100 nmol dopamine/l. The stimulatory effect of dibutyryl cyclic AMP (dbcAMP) on prolactin release was also tested. The relationship between dbcAMP and somatostatin was similar to that between TRH and somatostatin. When adenohypophyses of male rats were used for perifusion experiments, somatostatin (100 nmol/l) did not inhibit basal prolactin release from the fresh male pituitary in contrast with the primary cultured pituitary cells, but dopamine (1 μmol/l) effectively inhibited prolactin release.
In conclusion, (1) oestrogen converts the somatostatin-insensitive route into a somatostatin-sensitive route for basal prolactin release, (2) TRH-induced prolactin release passes through both somatostatin-sensitive and -insensitive routes, (3) dopamine blocks both somatostatin-sensitive and -insensitive routes and (4) cAMP activates both somatostatin-sensitive and -insensitive routes.
Journal of Endocrinology (1991) 130, 79–86
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ABSTRACT
Male rats showed maternal behaviour within 72 h after the onset of continuous exposure to newborn rat pups. The latency of the behavioural response could be reduced by daily treatment with the dopamine receptor antagonist domperidone (2 × 2·5 mg/rat), which increased serum prolactin concentrations (241·4 ± 26·5 (s.e.m.) μg/l) above those of vehicle-treated males exposed to pups (25·3 ± 11·7 μg/l). Male rats did not respond to exposure to pups by secreting prolactin; keeping endogenous prolactin concentrations at a minimum (2·8±0·1 μg/l) by daily treatment with the dopamine receptor agonist bromocriptine (0·5 mg/rat) did not affect the behavioural response of male rats to newborn pups. Neither exposure to pups nor the modest hyperprolactinaemia induced by daily domperidone treatment affected the display of male sexual behaviour by male rats.
J. Endocr. (1984) 102, 115–119
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Instituto de Neurobiologia, Serrano 665, Buenos Aires, Argentina
(Received 9 June 1977)
Changes in the levels of catecholamines in the hypothalamus during the oestrous cycle have been reported by Donoso, Stefano & Biscardi (1966) and Stefano & Donoso (1967). Shaar & Clements (1974) found that lower concentrations of dopamine and noradrenaline than those found in the hypothalamus can inhibit the release of prolactin from the rat pituitary gland. We have studied the levels of noradrenaline and dopamine in the median eminence around the time of the spontaneous preovulatory release of hormones.
Adult female Holtzman rats showing at least three consecutive 4 day cycles, were killed by decapitation at 09.30, 13.00 and 17.30 h on the days of dioestrus I and pro-oestrus. After decapitation, blood was collected into centrifuge tubes and the brains were immediately removed and frozen on solid CO2. Serum was separated by centrifugation and stored at −20 °C
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Department of Experimental Endocrinology, Institute of Endocrinology, Medical Academy of Łódź, Dr. Sterling str. 3, 91-425 Łódź, Poland
(Received 31 May 1977)
The secretory function of the intermediate lobe of the pituitary gland is under hypothalamic control (Howe, 1973; Hadley & Bagnara, 1975). Penny, Thody, Tilders & Smelik (1977) have suggested that the synthesis and release of melanocyte-stimulating hormone (MSH) is mediated by dopaminergic neurones which make synaptic contact with secretory cells in the pars intermedia (Björklund, Moore, Nobin & Stenevi, 1973). We have attempted to examine whether the dopaminergic mechanism is also involved in the control of the mitotic activity of the pars intermedia cells and have studied the effects of pimozide, a dopamine receptor blocker (Anden, Butcher, Corrodi, Fuxe & Ungerstedt, 1970) and 2-bromo-α-ergocriptine (bromo-criptine), a dopamine receptor agonist (Loew, Vigouret & Jaton, 1976) on the mitotic activity of the pars intermedia of the rat pituitary gland.
Twenty-three
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ABSTRACT
In this study we have examined the effects of TRH, thyroid hormones and dopamine on the rat anterior pituitary content of neuromedin U-like immunoreactivity. Oral administration of TRH (20 mg/100 g per day) to euthyroid animals evoked a fivefold increase in peptide content after 12 days of treatment. This effect was found to be dependent upon circulating levels of thyroid hormone, since administration of TRH to thyroidectomized animals failed to show a similar effect without simultaneous treatment with tri-iodothyronine. The possibility that the TRH-induced increase in anterior lobe neuromedin U content reflected alterations in prolactin secretion or synthetic rate was also examined. Treatment of euthyroid animals with a dopamine agonist and antagonist was, however, without effect. These results demonstrate a unique relationship between TRH and thyroid hormone levels in increasing the anterior lobe content of neuromedin U immunoreactivity.
Journal of Endocrinology (1989) 122, 471–476
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ABSTRACT
This study was conducted to determine whether photoperiod-induced changes in serum concentrations of prolactin in cattle were associated with changes in activity of dopamine or 5-hydroxytryptamine (5-HT) neurones in the infundibulum/pituitary stalk and the secretion rate and number of lactotrophs in the anterior pituitary gland.
Sixteen prepubertal bull calves (approximately 8 weeks of age) were divided into two groups. One group of eight was maintained on a photoperiod of 8 h light : 16 h darkness (8L : 16D) and the other group was exposed to 16L : 8D for 4 weeks. At this time calves were injected with a decarboxylase inhibitor (m-hydroxybenzylhydrazine dihydrochloride, NSD 1015) which blocks the conversion of dihydroxyphenylalanine (DOPA) to dopamine and of 5-hydroxytryptophan (5-HTP) to 5-HT. Calves were killed with pentobarbital 15 min later. Accumulations of DOPA and 5-HTP in selected brain regions were used as indices of activity of dopamine and 5-HT neurones respectively. Secretory rate and number of prolactinsecreting lactotrophs were determined by reverse haemolytic plaque assay.
Relative to calves exposed to 8L : 16D, exposure to 16L : 8D increased serum concentrations of prolactin by eightfold, anterior pituitary gland weight by 23%, release of prolactin from pituitary explants by 57% and the area of the plaque for prolactin-secreting lactotrophs by 70%. There was no difference in the rates of accumulation of DOPA and 5-HTP in the infundibulum/pituitary stalk of animals exposed to 4 weeks of 16L : 8D or 8L : 16D.
It was concluded that increased serum concentrations of prolactin in bulls exposed to a photoperiod of 16L : 8D for 4 weeks were associated with increased secretion of prolactin from lactotrophs which was not the result of a coincident reduction in activity of dopamine neurones or an activation of 5-HT neurones that terminate in the infundibulum/pituitary stalk.
Journal of Endocrinology (1991) 129, 141–148
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During suckling, anaesthetized lactating rats release regular (about every 7 min) but brief )ulses of oxytocin (0·5–1·0 mu.) which produce single transient increases in intramammary [unk]ressure. Drugs which selectively impair synaptic transmission were used to determine the [unk]ole of dopamine and noradrenaline in regulating this natural reflex. Diethyldithiocarbamate 100–200 mg/kg, i.v.) and α-methylparatyrosine (100–400 mg/kg, i.v.) which inhibit the [unk]ynthesis of catecholamines both blocked the suckling-induced release of oxytocin. The milk[unk]jection reflex was also inhibited in a dose-dependent manner by the intravenous administraion of the dopamine antagonists, fluphenazine (0·7 mg/kg), pimozide (1·4 mg/kg), cis-lupenthixol (4·5 mg/kg) and metoclopramide (6·0 mg/kg), and caused a significant inhibition P < 0·01) of the reflex in 50% of the rats tested. The α-adrenoceptor antagonist phenoxy[unk]enzamine (1·4 mg/kg) was similarly effective. Dopamine (40 μg), bromocriptine (10 μg), [unk]pomorphine (100 μg), noradrenaline (10 μg) and phenylephrine (2 μg) injected into the;erebral ventricles evoked a sustained release of oxytocin which produced multiple increases n intramammary pressure; isoprenaline (4 μg) was ineffective. The release of oxytocin evoked [unk]y dopamine and noradrenaline was prevented by cis-flupenthixol and phenoxybenzamine respectively. None of the drugs used affected the mammary sensitivity to exogenous oxytocin lor were their actions modified by pretreatment with propranolol (1 mg/kg). The results [unk]uggest that the neural pathway for the reflex release of oxytocin during suckling in the rat [unk]ontains both dopaminergic and noradrenergic synapses, the latter acting through α-[unk]drenoceptors and being distal in the pathway to the dopaminergic component.
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In Heteropneustes fossilis, administration of a single dose (0.15 micrograms/g body weight, i.p.) of [D-Ala6,Gly10]-gonadotrophin-releasing hormone analogue (GnRHa) induced ovulation (in 35 of 35 fish) when mild-stripped at 16 h. Plasma gonadotrophin II (GTH II) levels showed a highly significant increase at 2, 4, 8, 12 and 16 h with the peak at 8 h. Plasma cortisol, progesterone and testosterone showed significant elevations at 2, 4, 8 and 12 h with peaks at 8 h (cortisol and testosterone) and 4 h (progesterone). The levels declined to control values at 16 and 48 h except that of testosterone which decreased even further. In contrast, plasma levels of oestradiol-17 beta decreased significantly at 2, 4, 8 and 12 h, with the lowest value at 8 h, but increased at 16 and 18 h. The contents of hypothalamic and pituitary serotonin and noradrenaline increased at 8 h, coinciding with the peak GTH II rise, and decreased at 16 h. In contrast, dopamine content declined at 8 h in both the hypothalamus and pituitary, but increased at 16 h only in the hypothalamus. The hypothalamic adrenaline level decreased at 8 h but increased significantly at 16 h. Hypothalamic levels of monoamine oxidase, catechol O-methyltransferase and dopamine beta-hydroxylase were elevated significantly at 8 h; the dopamine beta-hydroxylase activity decreased at 16 h. Phenylethanolamine N-methyltransferase activity was elevated only at 16 h, coinciding with the rise in adrenaline content. It is inferred that the preovulatory decrease in dopamine content concomitant with rises in serotonin and noradrenaline levels, triggered by the low titre of oestradiol, might have potentiated the GnRHa/GnRH (endogenous)-induced release of GTH II for a prolonged period.
