Histaminergic Regulation of Prolactin Secretion: Involvement of Tuberoinfundibular Dopaminergic Neurons

Knigge, Ulrich; Matzen, Steen Henrik; Warberg, Jørgen

doi:10.1159/000125005

Cited by 15 publications

(7 citation statements)

References 14 publications

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“…The ACTH antiserum (generously provided by the National Pituitary Agency, National Institute of Health) does not cross-react with β-endorphin or β-LPH and has less than 0.4% cross-reactivity with α- and β-melanocyte stimulating hormone. Synthetic human ACTH [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39](generously provided by the National Pituitary Agency, National Institute of Health) served as reference preparation and iodination. The least detectable quantity of ACTH was 1 pmol/l plasma, and the intra- and interassay coefficients of variation were 4 and 5%.…”

Section: Methodsmentioning

confidence: 99%

“…The effect of HA on PRL secretion has been suggested to be mediated via an inhibition of tuberoinfundibular dopaminergic neurons, since HA decreased the concentration of dopamine in blood obtained from the long pituitary portal vessels in female and male rats [15, 16]. However, in other studies, HA did not affect the turnover of dopamine in the median eminence [17, 18].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Selective Blockade of Catecholaminergic Alpha and Beta Receptors on Histamine-Induced Release of Corticotropin and Prolactin

et al. 1999

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We investigated the role of adrenergic receptors in histamine (HA)-induced release of corticotropin (ACTH) and prolactin (PRL) in conscious male rats. Specific α- or β-receptor antagonists were administered intracerebroventricularly in doses of 1 mmol at time –20 min, and HA (270 nmol), the H₁ receptor agonist 2-thiazolylethylamine (2-TEA; 2,180 nmol) or the H₂ receptor agonist 4-methylHA (4-MeHA; 790 nmol) were administered intracerebroventricularly at –15 min. The animals were decapitated at 0 min, and plasma was analyzed for ACTH and PRL. Administration of HA and the histaminergic agonists stimulated ACTH secretion equally, while only HA and the H₂ receptor agonist stimulated PRL secretion. Pretreatment with the adrenergic receptor antagonists had no effect on the ACTH response to the histaminergic compounds. In contrast, the PRL response to HA or 4-MeHA was inhibited or prevented by the α-receptor antagonists phenoxybenzamine and phentolamine, the α₁-receptor antagonist prazocin, the β-receptor antagonist propranolol and the β₁-receptor antagonist atenolol, whereas the α₂-receptor antagonist yohimbine or the β₂-receptor antagonist ICI-118-551 had no effect. The study indicates that histaminergic neurons interact with the catecholaminergic neuronal system in regulation of PRL secretion, and that this interaction is dependent upon activation of α₁- and β₁-receptors. In contrast, histaminergic neurons stimulate ACTH secretion independently of adrenergic receptor activation.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of Selective Blockade of Catecholaminergic Alpha and Beta Receptors on Histamine-Induced Release of Corticotropin and Prolactin

et al. 1999

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“…Since both histaminergic and serotoninergic nerve fibers are widespread within the hypothalamic area [1,28,34,35], and since both transmitters appear to be involved in the mediation of the stress-induced PRL release [2,13,18], an interaction between these neuronal systems seems possible. Further more, it has previously been found that histamine interacts with tuberoinfundibular dopaminergic neurons [11,17,19]. The mediation of the PRL-stimulating action of histamine therefore seems to involve dopaminergic as well as seroto ninergic systems.…”

Section: Discussionmentioning

confidence: 89%

“…24. 33].It has been shown that the PRL stimulatory effect of his tamine involves inhibition of the tuberoinfundibular dopa minergic system, since histamine reduced the concentration of dopamine in pituitary portal blood [II,17], and since Received: June 10, 1987 Accepted after revision: March 25, 1988 blockade of dopamine receptors inhibited the PRL-reIeasing effect of histamine [17,19]. However, other hypo thalamic transmitter systems might also participate as me diators of the histamine-induced PRL release.…”

mentioning

confidence: 99%

Histaminergic Regulation of Prolactin Secretion: Involvement of Serotoninergic Neurons

Knigge

Sleimann²,

Matzen³

et al. 1988

Neuroendocrinology

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The possible involvement of the serotoninergic system in histamine-induced PRL secretion was studied in urethane anesthetized male rats. Intracerebroventricular infusion of histamine (30 µg) stimulated PRL secretion 10-fold. This effect was mimicked by the H₂-receptor agonist dimaprit (300 µg), while the H₁-receptor agonist 2-thiazolylethylamine (140 µg) had no effect. Pretreatment with the serotonin receptor blockers methysergide (2.5 mg/kg i.p.) or ketanserin (2.5 or 10.0 mg/kg i.p.) reduced the PRL peak response to histamine 75, 54, or 58%, respectively. During serotonin receptor blockade, dimaprit had a stimulatory effect similar to that of histamine, while 2-thiazolylethylamine had no effect. Intra-arterial infusion of histamine (420 µg) stimulated PRL secretion 6-fold. This effect was mimicked by the H₁-receptor agonist 2-thiazolylethylamine (1,900 µg), while the H₂-receptor agonist dimaprit (3,000 µg) had no effect. Pretreatment with methysergide (2.5 mg/kg i.p.) or ketanserin (2.5 or 10.0 mg/kg i.p.) reduced the peak response to histamine 54, 54, or 51%, respectively. The effect of histamine was mimicked by 2-thiazolylethylamine, while dimaprit slightly inhibited the PRL secretion. The antiserotoninergic activity of methysergide and ketanserin was demonstrated by their ability to prevent the PRL-releasing effect to serotonin. The effects of methysergide and ketanserin were not due to dopamine-like activity, since none of the drugs affected basal PRL secretion and since the dopamine receptor antagonist pimozide did not prevent the inhibitory effect of methysergide on the histamine-induced PRL release. The findings indicate that histamine-stimulated PRL secretion is mediated in part by serotoninergic neurons.

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“…The effect of HA on ACTH secretion is caused by an effect on corticotropinreleasing hormone neurons and vasopressin (AVP) neurons in the paraventricular nucleus (7-9) -probably via an interaction with prostaglandins (10). The effect of HA on PRL secretion seems to involve AVP and serotonin (11,12), while the involvement of dopamine is in question (13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

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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Histaminergic Regulation of Prolactin Secretion: Involvement of Tuberoinfundibular Dopaminergic Neurons

Cited by 15 publications

References 14 publications

Effect of Selective Blockade of Catecholaminergic Alpha and Beta Receptors on Histamine-Induced Release of Corticotropin and Prolactin

Effect of Selective Blockade of Catecholaminergic Alpha and Beta Receptors on Histamine-Induced Release of Corticotropin and Prolactin

Histaminergic Regulation of Prolactin Secretion: Involvement of Serotoninergic Neurons

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

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