Adrenoceptors in the preoptic-anterior hypothalamic area stimulate secretion of prolactin but not growth hormone in the male rat

Willoughby, John O.; Day, Trevor A.; Menadue, Margaret; Jervois, P.M.; Blessing, W.W.

doi:10.1016/0361-9230(86)90141-3

Cited by 23 publications

(26 citation statements)

References 43 publications

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“…The catecholamines E and NE significantly increased PRL secretion in accordance with the generally stimulatory role of catecholamines in the central regulation of PRL secretion (23,24,37). The stimulatory effect of E on PRL secretion was not affected by any of the histaminergic compounds.…”

Section: Discussionsupporting

confidence: 72%

Effect of blockade of postsynaptic H1 or H2 receptors or activation of presynaptic H3 receptors on catecholamine-induced stimulation of ACTH and prolactin secretion

Willems¹,

Knigge

Jørgensen³

et al. 2000

European Journal of Endocrinology

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The effect of inhibition of the neuronal histaminergic system by blockade of postsynaptic H1 or H2 receptors or activation of presynaptic H3 autoreceptors on the ACTH and prolactin responses to the catecholamines epinephrine and norepinephrine was investigated in conscious male rats. Intracerebroventricular infusion of epinephrine and norepinephrine stimulated ACTH and prolactin secretion. Prior intracerebroventricular infusion of the H1 receptor antagonist, mepyramine, or the H2 receptor antagonist, cimetidine, had no effect on the ACTH response to epinephrine or norepinephrine, while these responses were inhibited by pretreatment with the H3 receptor agonist, imetit. The prolactin response to norepinephrine was significantly inhibited by pretreatment with mepyramine, cimetidine or imetit whereas the three histaminergic compounds had no effect on the prolactin response to epinephrine. The findings suggest that the histaminergic system exerts a mediating or permissive action on the norepinephrine-induced stimulation of prolactin secretion, whereas an intact histaminergic system may not be required for catecholamines to stimulate ACTH secretion. The inhibitory effect of imetit on catecholamine-induced release of ACTH may be due to an activation of H3 receptors located presynaptically on non-histaminergic neurons, e.g. aminergic neurons. The study further indicates an important role of histamine in the neuroendocrine regulation of prolactin secretion.

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Section: Discussionsupporting

confidence: 72%

Effect of blockade of postsynaptic H1 or H2 receptors or activation of presynaptic H3 receptors on catecholamine-induced stimulation of ACTH and prolactin secretion

Willems¹,

Knigge

Jørgensen³

et al. 2000

European Journal of Endocrinology

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“…and the reverse is true for serotonin (37), indicating that independent effects are observed after injections in either site. We have also established previously that reproducible effects of a repeat injection are seen, on prolactin for example, with a first and an eighth injection (38), although in this study, animals received no more than six injections. Of necessity, different animals contributed to the groups used for different dosages of agonist.…”

Section: Methodssupporting

confidence: 56%

“…Injections described below were made using 30 gauge injection needles inserted through the guide cannulae until they reached the skull. The level of the injection needles ensured that the opening of the needles was 0.5 mm above the (36)(37)(38).…”

Section: Methodsmentioning

confidence: 99%

Intrahypothalamic Mu‐, not Delta‐ or Kappa‐Opioid Receptor Activation Causes Growth Hormone Secretion

Willoughby¹,

Kapoor²,

Mackenzie³

1991

J Neuroendocrinology

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Key words: growth hormone, mu-, kappa-and delta-opioid receptors, basal and anterior hypothalamus. AbstractThe possible effects of opioid receptor agonists on growth hormone (GH)-releasing factor or somatostatin neurons were examined by measuring the effects of localized intracerebral injections of mu-, delta-and kappa-selective agonists on GH secretion, Serial GH concentrations were measured in plasma in unanaesthetized male rats chronically prepared with venous and intracerebral cannulae, before and after treatment with bilateral intracerebral injections of opioid agonists in the preoptic anterior hypothalamic area and medial basal hypothalamus.In the medial basal hypothalamus, injections of the mu-agonist DAGO (Tyr-D-Ala-Gly-(Me)Phe-Gly-ol) caused dose-responsive increases in GH, the maximally effective dose being 0.001 nmoles. Injection of 10,000-fold higher doses of the delta-agonist DPDPE ([D-Pen,D-Penlenkephalin) and the kappa-agonist U50,488H were also effective in stimulating GH secretion. In the preoptic anterior hypothalamic area, DAGO caused dose-responsive increases in GH, the maximally effective dose being 0.01 nmoles. U50,488H was ineffective at 1,000-fold higher doses while DPDPE was effective at 100-to 1,000-fold higher doses.We conclude that hypothalamic mu-opioid receptor activation on or near somatostatin or GH-releasing factor neurons causes GH secretion, Opioids capable of acting on other opioid receptors may also stimulate GH secretion, though only at doses that seem likely to affect mu-receptors.The phenomenon of pulsatile growth hormone (GH) secretion is recognized to be a consequence of the net rhythmic stirnulatory action of somatostatin and GH-releasing factor (GRF) at the somatotroph (1-3). Somatostatin-and GRF-containing neurons are located in the periventricular preoptic/anterior hypothalamic area (PO/AHA) and arcuate nucleus in the medial basal hypothalamus (MBH), respectively (4-8). It has seemed probable from systemic and intracerebroventricular pharmacological studies that GH-regulating neurons are potently affected by opiates which usually cause marked stimulation of G H secretion. It has not clearly been demonstrated whether opioids act on somatostatin or G R F neurons or both. The present study uses a functional approach to determine possible actions of opioid receptor agonists on somatostatin-or GRF-containing neurons by measuring the effects on G H secretion of direct intrahypothalamic microinjections of opioid receptor agonists in the PO/AHA or MBH. The ligands we used in these experiments were highly selective for their receptor subtypes as shown by James and Goldstein (9), Tyr-D-Ala-Gly-(Me)PheGly-ol (DAGO) being 130 times more selective for mu than delta sites and 170 times more selective for mu than kappa. Similarly, [D-Pen,D-Penlenkephalin (DPDPE) is more selective for deltathan mu-(780 times) or kappa-receptors (430 times) and US0,488H is more selective for kappa-than mu-(1,300 times) o r delta-receptors (12,000 times) (9). Results P O / A H A injectionsRinger injec...

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“…Indeed, in several animal and human studies a possible adrenergic control of PRL release has been suggested. In rat studies, infusion of adrenaline into the preoptic hypothalamic area or into the lateral cerebral ventricle enhanced PRL output and the effect was blocked by phentolamine [68, 69]. In humans, intravenous infusion of the α 1 -agonist methoxamine that can cross the blood-brain barrier stimulates PRL secretion [70].…”

Section: Discussionmentioning

confidence: 99%

Mirtazapine Decreases Stimulatory Effects of Reboxetine on Cortisol, Adrenocorticotropin and Prolactin Secretion in Healthy Male Subjects

Schüle

Baghai²,

Laakmann³

2004

Neuroendocrinology

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Reboxetine is a selective noradrenaline reuptake inhibitor, whereas mirtazapine acts as an antagonist at noradrenergic α₂, serotonin (5-HT₂), 5-HT₃ and histamine H₁ receptors. In a former study we could demonstrate an inhibitory impact of mirtazapine on cortisol secretion. In the present investigation, the influence of combined administration of 15 mg mirtazapine and 4 mg reboxetine on the cortisol (COR), adrenocorticotropin (ACTH), growth hormone (GH), and prolactin (PRL) secretion was examined in 12 healthy male subjects, compared to reboxetine alone (4 mg). In a randomized order, the subjects received reboxetine (4 mg) alone or the combination of reboxetine (4 mg) and mirtazapine (15 mg) at 8:00 a.m. on two different days. After insertion of an intravenous catheter, blood samples were drawn 1 h prior to the administration of single reboxetine or the combination (reboxetine and mirtazapine), at time of administration, and during the time of 5 h thereafter in periods of 30 min. Serum concentrations of COR, GH, and PRL as well as plasma levels of ACTH were determined in each blood sample by means of double antibody RIA, fluoroimmunoassay and chemiluminescence immunometric assay methods. The area under the curve (AUC) was used as parameter for the COR, ACTH, GH, and PRL response. For statistical evaluation, the Wilcoxon signed-ranks test was performed. There was a pronounced stimulation of COR, ACTH, GH, and PRL concentrations after single administration of reboxetine. When reboxetine was given in combination with mirtazapine, a significant reduction of the COR, ACTH, and PRL stimulation was observed whereas GH secretion patterns remained unchanged, compared to single administration of reboxetine. Apparently, the stimulatory effects of reboxetine on pituitary hormone secretion via noradrenergic mechanisms are counteracted in part by the α₂-blocking properties of mirtazapine and its inhibitory influence on cortisol secretion.

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Adrenoceptors in the preoptic-anterior hypothalamic area stimulate secretion of prolactin but not growth hormone in the male rat

Cited by 23 publications

References 43 publications

Effect of blockade of postsynaptic H1 or H2 receptors or activation of presynaptic H3 receptors on catecholamine-induced stimulation of ACTH and prolactin secretion

Effect of blockade of postsynaptic H1 or H2 receptors or activation of presynaptic H3 receptors on catecholamine-induced stimulation of ACTH and prolactin secretion

Intrahypothalamic Mu‐, not Delta‐ or Kappa‐Opioid Receptor Activation Causes Growth Hormone Secretion

Mirtazapine Decreases Stimulatory Effects of Reboxetine on Cortisol, Adrenocorticotropin and Prolactin Secretion in Healthy Male Subjects

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