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Hospital General de Agudos J. M. Ramos Mejía, Buenos Aires, Argentina
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Turku Center for Disease Modeling, University of Turku, Turku, Finland
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Department of Surgery and Cancer, Imperial College London, London, UK
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that hyperprolactinemia is the main cause for the reproductive defects of adult hCGβ+ females, which can be prevented by a short-term treatment with the dopamine agonist cabergoline at the beginning of the reproductive age ( Ratner et al. 2012
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overactivation and progression of HF is less well known. Circulating catecholamines, comprising dopamine (DA), norepinephrine (NE) and epinephrine (EPI), are primarily synthesized and released from the chromaffin cells of the adrenal medulla ( Goldstein et al
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SUMMARY
The neurohaemal part of the median eminence of the rat hypothalamus is characterized by numerous nerve terminals which end near a rich network of fenestrated capillaries. An attempt was made to isolate different types of nerve terminals by means of sucrose density-gradient centrifugation. The subcellular fractions obtained were assayed for dopamine, noradrenaline and 5-hydroxytryptamine. In addition FSH- and GH-releasing activities were determined. A sample of each fraction obtained was taken for electron microscopical observations.
Dopamine, noradrenaline, 5-hydroxytryptamine, GH- and FSH-releasing factors were present in higher concentration in the nerve endings. A further fractionation showed that noradrenaline was present in the lightest synaptosomal band, dopamine in the middle one, and 5-hydroxytryptamine in the heaviest. GH-RF and FSH-RF were recovered mainly from the band containing dopamine. The relevance of this localization to the physiological role of the median eminence is discussed.
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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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pharmacologic modulators of dopamine signaling or GHSR agonist. First, we assessed the locomotor response to amphetamine (AMPH), a psychoactive drug known to reverse dopamine transporter activity at post-synaptic target leading to enhanced dopamine (DA) release
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of early-stage T2DM, insulin resistance was observed while dopamine release was attenuated and dopamine clearance was diminished in the basal ganglia, indicating that dopaminergic signalling is compromised in T2DM ( Morris et al . 2011 ). This
Department of Endocrinology, CI Parhon National Institute of Endocrinology, Department of Endocrinology, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania
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can be considered for this use in selected cases. For instance, in ACM patients with severe DM, its use could be safer due to its favourable impact on glycemic control ( Barkan et al . 2005 ). Dopamine agonists Dopamine agonists (DA) are efficacious
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School of Medicine, State Key Laboratory for Medical Genomics, Laboratory of Development and Diseases, Shanghai Institute of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine and Metabolic Disease
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) respectively. Therefore, it is intriguing to investigate the anatomic relationship between CHGA -expressing cells and the interrenal cells/pronephros during embryogenesis by double in situ hybridization assay. Furthermore, in humans, dopamine
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Hyperprolactinaemia produced in rats by the transplanted prolactin-secreting tumours MtTW15 and 7315a significantly (P<0·01) inhibited by 70% the incorporation of [3H]thymidine into the pituitary DNA of the host animals. The weight and the DNA content of the glands were significantly (P<0·01) reduced by 30%. The administration of haloperidol, a dopamine receptor blocking agent, to the tumour-bearing rats increased the suppressed DNA replication in the anterior pituitary glands by approximately 560% in the MtTW15-bearing rat and by 100% in the 7315a-bearing animals. Furthermore, injection of drugs which stimulate prolactin release either by blocking the synthesis of dopamine (α-methyl-p-tyrosine) or the re-uptake of dopamine (reserpine) stimulated DNA synthesis by 800 and 100% respectively in the anterior pituitary gland of rats bearing the MtTW15 tumour. In contrast, lisuride, a dopamine agonist, significantly inhibited the incorporation of [3H]thymidine into the DNA of the pituitary gland of normal but not hyperprolactinaemic rats. Chronically administered oestrogens to hyperprolactinaemic rats increased the weight (100%), DNA content (31%), incorporation of [3H]thymidine into DNA (680%) and synthesis and release of prolactin (300%) in the pituitary gland.
The incorporation of [3H]thymidine into tumour DNA was several times higher than in the pituitary gland of the host animal and was not significantly modified by any of the above treatments. Likewise the hyperprolactinaemia of the tumour-bearing rats was not significantly changed.
In conclusion, we have shown that hyperprolactinaemia inhibits DNA synthesis in the anterior pituitary gland and this inhibition can be reversed completely by a dopamine receptor blocking agent and by hypothalamic dopamine depleting drugs. We propose that dopamine regulates, either directly or indirectly, DNA synthesis in the lactotrophs of the pituitary gland, which may be responsive to negative feedback mechanisms.
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ABSTRACT
In goldfish, dopamine acts as an endogenous inhibitor of basal and gonadotrophin-releasing hormone (GnRH)-stimulated gonadotrophin release. The purpose of the present study was to investigate the effects of dopamine on the pituitary GnRH receptors in vivo and in vitro in goldfish. The goldfish pituitary contains two classes of GnRH-binding sites, a high-affinity/low-capacity site and a low-affinity/high-capacity site. Injection of domperidone, a dopamine antagonist, resulted in a dose- and time-related increase in capacity of both the high- and low-affinity GnRH-binding sites; apomorphine, a dopamine agonist, completely reversed this effect. The effects on GnRH receptor capacity correlated very closely with changes in serum gonadotrophin concentrations. Domperidone was generally without effect on GnRH-binding affinity; however, a small but significant decrease in affinity was observed for the low- affinity binding site at 18 h after injection of the highest dose of domperidone used (40 μmol/kg body weight). Treatment with apomorphine of goldfish pituitary fragments in a perifusion system caused a decrease in the capacity of both the high- and low-affinity GnRH-binding sites without affecting binding affinity; domperidone reversed this effect. It is concluded that the dopaminergic inhibition of basal and GnRH-stimulated gonadotrophin release in goldfish might, in part, be the result of a down-regulation of the pituitary GnRH receptors; this effect of dopamine can be achieved by a direct action at the pituitary level.
Journal of Endocrinology (1989) 121, 239–247
