Role of histamine in the increased secretion of prolactin induced by ether in adult male rats

Alvarez, Edgardo O.

doi:10.1677/joe.0.0950409

Cited by 17 publications

(6 citation statements)

References 13 publications

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“…In contrast, intracerebroventricularly administered HA may have a more localized effect in restricted hypothalamic areas where it stimulates primarily H2 receptors. This hypothesis is supported by an earlier finding [1] that the PRL response to ether stress was inhibited by only H2 receptor antagonists following intracerebroventricular infusion and inhibited by both H2 and Hi receptor antagonists following their injec tion into the preoptic area.…”

Section: Discussionsupporting

confidence: 76%

Histaminergic Mediation of the Stress-Induced Release of Prolactin in Male Rats

Knigge

Matzen²,

Warberg³

1988

Neuroendocrinology

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Histamine (HA) is likely to participate in the neuroendocrine regulation of prolactin (PRL) secretion. We, therefore, studied the possible involvement of HA in the stress-induced release of PRL in conscious male rats. HA (30 µg) infused intracerebroventricularly 15 min before decapitation elevated PRL plasma levels from 5 + 1 to 54 ± 6 ng/ml (p < 0.01). Intracerebroventricular infusion of the H₂ receptor antagonists cimetidine (CIM; 100 µg) or ranitidine (RAN; 125 µg) abolished the PRL response to HA (p < 0.01), while intracerebroventricular infusion of the H₁ receptor antagonist mepyramine (MEP; 100 µg) inhibited the response only 40% (p < 0.05). Intra-arterial infusion of CIM (2,000 µg) or RAN (2,500 µg) inhibited the HA-stimulated PRL secretion 52% (p < 0.01) or 63% (p < 0.01), respectively. The H₁ receptor antagonists MEP (1,000 µg) and SKF-93944 (1,500 µg) had no effect following intra-arterial administration. Restraint stress increased the PRL level to 84 ± 6 ng/ml (p < 0.01 vs. control). This effect was prevented by intracerebroventricular infusion of CIM or RAN (p < 0.01) and inhibited 75% by MEP (p < 0.01). Intra-arterial infusion of CIM, MEP, and SKF-93944 inhibited the stress response about 50% (p < 0.01), while RAN decreased the response only 25% (p < 0.05). Ether stress elevated the plasma PRL concentration to 46 ± 5 ng/ml (p < 0.01 vs. control). When infused intracerebroventricularly, CIM or RAN prevented the response (p < 0.01), while MEP had no effect. Intra-arterial infusion of CIM or RAN attenuated the response approximately 50% (p < 0.01), while intra-arterial infusion of MEP or SKF-93944 inhibited the response 80% (p < 0.01). We conclude that restraint as well as ether stress stimulates the secretion of PRL via release of neuronal HA. The effect of HA seems primarily mediated through activation of H₂ receptors, whereas H₁ receptors appear to play a minor role.

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Section: Discussionsupporting

confidence: 76%

Histaminergic Mediation of the Stress-Induced Release of Prolactin in Male Rats

Knigge

Matzen²,

Warberg³

1988

Neuroendocrinology

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“…On the other hand, the POA-AHA is the site of control for the positive action of estradiol on PRL and the histaminergic sensitive locus for the ether stressinduced release of this hormone (Neill, 1972;Caligaris and Taleisnik, 1977;Kawakami and Yokohama, 1981;Alvarez, 1982). Histamine immunoreactive fibers and neurons has been described in this area (Wilcox and Seybold, 1982;Panula etal., 1984;Wouterlood and Gaykema, 1988;Inagaki, 1988) and HA sensitive sites evoking the PRL release were also reported (Alvarez and Donoso, 1981;Alvarez, 1982;Alvarez, 1984). It has been assumed that these HA-sensitive sites in the POA-AHA could mediate also LH release, by affecting the LH-RH output.…”

Section: Introductionmentioning

confidence: 99%

The probable role of histamine in the rostral hypothalamus on the prolactin and luteinizing hormone release induced by estrogen in conscious spayed rats

Horno¹,

Alvarez²

1989

J. Neural Transmission

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The participation of histamine (HA) sensitive sites in the preoptic-anterior hypothalamic area (POA-AHA) on prolactin (PRL) and luteinizing hormone (LH) surge induced by estrogen was studied in ovariectomized rats. Different groups of animals were subjected to the following experimental schedule: On day "0" rats were stereotaxically implanted into the POA-AHA with microinjection cannulae. On day "1", rats were injected s.c. with estrogen. On days "2" and "3", animals were microinjected into the POA-AHA with different drugs, according to the type of experiment, and at day "4", through a silastic cannula implanted previously in the jugular vein, blood samples were taken each hour between 15:00-21:00 h. In the plasma, PRL and LH concentrations were measured by RIA. Four experiments were performed. In Experiment 1, animals at 12:00 h were injected into the POA-AHA with pyrilamine maleate (an H 1-histamine antagonist), metiamide (an H2-histamine antagonist) or saline as control. In Experiment 2, rats at 12:00 h were injected into the POA-AHA with alpha-fluormethyl-histidine (an inhibitor of histamine synthesis) or the combined administration of pyrilamine and metiamide. In Experiment 3, rats previously microinjected with the histamine synthesis inhibitor were microinjected with 4-methyl-histamine (an H 2-histamine agonists) or 2-pyridilethyl-amine (an H 1-histamine agonist) and in Experiment 4, rats were microinjected at 09:00 h with metiamide, pyrilamine, fluor-methyl-histidine or saline as control. Results showed that in animals treated with pyrilamine or metiamide at noon the prolactin surge induced by estrogen was affected (inhibited by metiamide and shortened by pyrilamine, Experiment 1) and LH surge slightly affected. Rats that received FMH or the combined administration of the histamine antagonists the prolactin and LH surge were abolished (Experiment 2). Only the treatment of the H 2-histamine agonist was able to reproduce the prolactin increase in rats treated with FMH. Nor the H 1 or H 2-histamine agonists were effective in reproducing the LH surge in these animals (Experiment 3). Animals that received saline at 09:00 h into the POA-AHA, the prolactin and LH surges were abolished. Results confirm that histamine in the POA-AHA is important for the expression of prolactin and LH surge induced by estrogen and suggest that H 1- and H 2-histamine receptors are involved in the complex timing mechanisms of the rostral hypothalamus that control both hormone release in rats.

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“…In a further experiment, we attempted to define whether a-MHA may act through modifications in histaminergic function or directly at postsynaptic sites. For that purpose, animals were pretreated with the irrevers-ible HA synthesis inhibitor a-fluoromethylhistidine (a-FMHIS), a drug that depletes the neuronal pool of HA in the brain [9][10][11].…”

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confidence: 99%

Stimulation of H<sub>3</sub>-Histamine Receptors Increases the Release of Prolactin in Male Rats

Navarro

Otoya²,

Donoso³

1993

Neuroendocrinology

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Histamine (HA) stimulates prolactin secretion via H₁ and H₂ receptors. In the present study, we examined the role of a third subtype of receptor recently described in brain, the H₃-HA receptor, on prolactin secretion in male rats. R(-)α-methyl-HA (α-MHA), a selective H₃ receptor agonist, was injected into the lateral ventricle of the brain in freely moving rats. α-MHA produced a dose-dependent (1-5 µg) and long-lasting increase in plasma prolactin levels. This increase was observed from 15 to 60 min after injection of α-MHA. Its stimulatory action was prevented by thioperamide (20 µg i.v.t), a selective H₃ antagonist. This compound, injected intraventricularly, lacked effect by itself on basal plasma prolactin levels. Neither pyrilamine (Hi antagonist; 60 µg i.v.t.) nor ranitidine (H₃ antagonist; 60 µg i.v.t.) affected α-MHA-induced prolactin release. The stimulatory effect was still present when brain HA was depleted by α-fluoromethylhistidine (30 mg/kg i.p.). Our findings suggest that α-MHA evokes prolactin release by activation of postsynaptic H₃ receptors.

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Role of histamine in the increased secretion of prolactin induced by ether in adult male rats

Cited by 17 publications

References 13 publications

Histaminergic Mediation of the Stress-Induced Release of Prolactin in Male Rats

Histaminergic Mediation of the Stress-Induced Release of Prolactin in Male Rats

The probable role of histamine in the rostral hypothalamus on the prolactin and luteinizing hormone release induced by estrogen in conscious spayed rats

Stimulation of H<sub>3</sub>-Histamine Receptors Increases the Release of Prolactin in Male Rats

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