Interactions of Histaminergic and Serotonergic Neurons in the Hypothalamic Regulation of Prolactin and ACTH Secretion

Jørgensen, Henrik; Knigge, Ulrich; Kjær, Andreas; Warberg, Jørgen

doi:10.1159/000127136

Cited by 19 publications

(14 citation statements)

References 10 publications

(11 reference statements)

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“…This indicates that the posterior hypothalamus is involved in the mediation of the serotonergic stimulation of PRL secretion whereas an intact posterior hypothalamus is not required for induction of an ACTH and β-END response to serotonergic neuronal activation. The present results are similar to our finding that inhibition of neuronal HA synthesis or release or blockade of postsynaptic H 1 or H 2 receptors decreased the PRL response but not the ACTH response to serotonergic neuronal activation induced by 5-HTP and fluoxetine [37], present study] further suggesting that the effect of posterior hypothalamic lesion was due to destruction of histaminergic neurons. Furthermore, the preservation of the ACTH and β-END responses to serotonergic neuronal activation in lesioned animals indicates that the serotonergic neuronal system was not destroyed by the lesion, eliminating the possibility that the reduced hormone responses in the animals exposed to stress or LPS was due to damage of serotonergic nerve fibers.…”

Section: Discussionsupporting

confidence: 93%

“…serotonergic, dopaminergic, catecholaminergic) neurons in the brain, whereby they mediate inhibition of the release of HA or other amines [23, 24, 34, 35, 36]. However, we have recently found that the H 3 receptor agonists do not participate in the hormone response to serotonergic neuronal activation [37]. The present results suggest that the inhibitory effect of H 3 receptor activation is caused via an action on presynaptic receptors located on histaminergic neurons rather than on other aminergic neurons, since their effect of the H 3 receptor agonists was similar to that induced by suppression of neuronal HA synthesis by α-FMH and blockade of postsynaptic H 1 or H 2 receptors [17, 18, 19, 20, 21].…”

Section: Discussionmentioning

confidence: 99%

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Stress-Induced Release of Anterior Pituitary Hormones: Effect of H<sub>3</sub> Receptor-Mediated Inhibition of Histaminergic Activity or Posterior Hypothalamic Lesion

Knigge¹,

Søe‐Jensen²,

Jørgensen³

et al. 1999

Neuroendocrinology

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The effect of stress- or lipopolysaccharide (LPS) endotoxin-induced release of ACTH, β-endorphin (β-END) and prolactin (PRL) was investigated in two groups of conscious male rats: (1) Rats pretreated with different H₃ receptor agonists, which inhibit neuronal histamine (HA) synthesis and release, and (2) rats with bilateral posterior hypothalamic lesion, which destroys the histaminergic perikarya exclusively localized in the mammillary nuclei. The H₃ receptor agonists R(α)methyl-HA, BP 2-94 or imetit injected intraperitoneally (ip) had no effect on basal secretion of ACTH or PRL but inhibited the ACTH and PRL responses to restraint stress and the ACTH response to LPS endotoxin. LPS had no effect on PRL secretion. The inhibitory effect of the agonists was prevented by prior ip administration of the H₃ receptor antagonist thioperamide. Bilateral lesion of the posterior hypothalamus inhibited the ACTH, β-END and PRL responses to restraint stress, ether stress and LPS endotoxin, whereas sham operation had no effect compared to nonoperated control rats. In addition, posterior hypothalamic lesion inhibited the PRL response but not the ACTH and β-END responses to activation of serotonergic neurons induced by ip administration of the 5-HT precusor 5-hydroxytryptophan in combination with the 5-HT re-uptake inhibitor fluoxetine. Thus, serotonergic pathways were not damaged by the lesions. The present results support our previous findings that inhibition of neuronal HA synthesis by α-fluoromethylhistidine as well as blockade of H₁ or H₂ receptors inhibit the ACTH, β-END and PRL responses to stress and LPS endotoxin and further substantiate an important role of histaminergic neurons in the mediation of the stress-induced release of pituitary stress hormones. Furthermore, in accordance with our previous findings, the lesion experiments indicated the existence of an interaction between the histaminergic and serotonergic system in regulation of the stress- and LPS-induced PRL release.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Stress-Induced Release of Anterior Pituitary Hormones: Effect of H<sub>3</sub> Receptor-Mediated Inhibition of Histaminergic Activity or Posterior Hypothalamic Lesion

Knigge¹,

Søe‐Jensen²,

Jørgensen³

et al. 1999

Neuroendocrinology

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“…However, in other studies, HA did not affect the turnover of dopamine in the median eminence [17, 18]. Other studies have indicated that the effect of HA is mediated via an interaction with vasopressinergic as well as serotonergic neurons [14, 19, 20, 21]. …”

Section: Introductionmentioning

confidence: 86%

“…In addition, we have recently found that HA interacts with prostaglandins but not with serotonin (5-HT) in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis [13, 14]. …”

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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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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“…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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Interactions of Histaminergic and Serotonergic Neurons in the Hypothalamic Regulation of Prolactin and ACTH Secretion

Cited by 19 publications

References 10 publications

Stress-Induced Release of Anterior Pituitary Hormones: Effect of H<sub>3</sub> Receptor-Mediated Inhibition of Histaminergic Activity or Posterior Hypothalamic Lesion

Stress-Induced Release of Anterior Pituitary Hormones: Effect of H<sub>3</sub> Receptor-Mediated Inhibition of Histaminergic Activity or Posterior Hypothalamic Lesion

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

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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