Neuronal histamine and expression of corticotropin-releasing hormone, vasopressin and oxytocin in the hypothalamus: relative importance of H1 and H2 receptors

Kjær, Andreas; Larsen, Philip J.; Knigge, Ulrich; Jørgensen, Henrik; Warberg, Jørgen

doi:10.1530/eje.0.1390238

Cited by 50 publications

(33 citation statements)

References 37 publications

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“…Histamine, upon binding to various kinds of histamine receptors (Hill 1990, Liu et al 2001, plays an important role in the regulation of several physiological processes such as vasodilation, smooth muscle contraction, gastric acid secretion, immune regulation and embryogenesis (Rokita et al 1992, Nissinen et al 1995, Hunyadi et al 1998. Besides these, its participation in neuroendocrine regulation has been described formerly (Knigge & Warberg 1991, Kjaer et al 1998. In mammals histaminergic neurons arise from the tuberomamillary nucleus of the hypothalamus to innervate corticotropinreleasing hormone-secreting neurons in the paraventricular and supraoptic nuclei as well as luteinizing hormone (LH)-releasing hormone-secreting neurons in the supraoptic nucleus of the hypothalamus.…”

Section: Introductionmentioning

confidence: 99%

“…In mammals histaminergic neurons arise from the tuberomamillary nucleus of the hypothalamus to innervate corticotropinreleasing hormone-secreting neurons in the paraventricular and supraoptic nuclei as well as luteinizing hormone (LH)-releasing hormone-secreting neurons in the supraoptic nucleus of the hypothalamus. Arginine vasopressin secretion is under histamine control as well (Kjaer et al 1998). Histamine does not act directly on the adenohypophysis (Knigge et al 1985), its influence on tropic hormones is expressed through its effect on the secretion of the trophormone-releasing hormones.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Histidine decarboxylase deficiency in gene knockout mice elevates male sex steroid production

Pap¹,

Rácz²,

Kovacs³

et al. 2002

Journal of Endocrinology

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Histamine is synthesized in cells by histidine decarboxylase (HDC). HDC-deficient knockout (KO) mice lack functional HDC and histamine in the tissues. In the present study we used this in vivo model for studying the role of HDC deficiency in the regulation of male steroid hormone metabolism.In agreement with earlier studies showing the lack of effects of central histamine on the basal secretion of gonadotrope hormones, we found no difference with in situ hybridization in the expression of GnRH in the hypothalamus of wild type and KO mice.The tissue concentrations of testosterone and several androgenic steroids were significantly elevated in the testes but not in the adrenal glands of HDC-KO mice. In contrast, serum estradiol levels failed to show a significant difference between the two groups. The weight of the testes was significantly smaller in both 7-day-old and adult KO mice. The ultrastructure of the adult testis indicated elevated steroid synthesis with more tightly coiled membranous whorls in Leydig cells.The present results suggest that changes in reproductive functions and sex steroid secretion in male HDC-KO mice are not due to altered hypothalamic GnRH expression but are probably related to definite modifications during fetal development of KO mice reinforced later by the lack of the effect of peripheral histamine. This may provide in vivo evidence that peripheral histamine is an important regulatory factor of male gonadal development during embryogenesis and of sex steroid metabolism later in adulthood.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Histidine decarboxylase deficiency in gene knockout mice elevates male sex steroid production

Pap¹,

Rácz²,

Kovacs³

et al. 2002

Journal of Endocrinology

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“…Histaminergic neurons make synaptic contact with OT neurons (40), and central administration of HA increases systemic OT release (4,19), OT mRNA levels (20), and c-fos expression in OT containing neurons (21). Blockade of central H1 receptors delays delivery of rat pups during parturition (26).…”

mentioning

confidence: 99%

Differential sensitivity of intranuclear and systemic oxytocin release to central noradrenergic receptor stimulation during mid- and late gestation in rats

Lipschitz¹,

Crowley²,

Bealer³

2004

American Journal of Physiology-Endocrinology and Metabolism

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Differential sensitivity of intranuclear and systemic oxytocin release to central noradrenergic receptor stimulation during mid-and late gestation in rats. Am J Physiol Endocrinol Metab 287: E523-E528, 2004. First published May 18, 2004 10.1152/ajpendo.00572.2003.-A number of changes occur in the oxytocin (OT) system during gestation, such as increases in hypothalamic OT mRNA, increased neural lobe and systemic OT, and morphological and electrophysiological changes in OT-containing magnocellular neurons, suggestive of altered neuronal sensitivity, which may be mediated by ovarian steroids. Because central norepinephrine (NE) and histamine (HA) are potent stimulators of OT release during parturition and lactation, the present study investigated the effects of central noradrenergic and histaminergic receptor activation on systemic (NE, HA) and intranuclear (NE) OT release in pregnant rats and in ovariectomized rats treated with ovarian steroids. Plasma OT levels in late gestation were significantly higher compared with all other groups, and neither adrenergic nor histaminergic receptor blockade decreased these elevated levels. Furthermore, the ␣-adrenergic agonist phenylephrine, but not histamine, stimulated systemic OT release to a significantly greater extent in late gestation than in midpregnant, ovariectomized, or steroid-treated females. Although basal extracellular OT levels in the paraventricular nucleus, as measured with microdialysis, were unchanged during pregnancy or steroid treatment, noradrenergic receptor stimulation of intranuclear OT release was significantly elevated in midgestation females compared with all other groups. These studies indicate that sensitivity of intranuclear and systemic OT release to noradrenergic receptor activation differentially varies during the course of gestation. pregnancy; neurotransmitter; norepinephrine; histamine; estradiol; progesterone PREVIOUS STUDIES HAVE SHOWN that central and systemic oxytocin (OT) release is important during parturition and lactation. OT is synthesized in hypothalamic magnocellular paraventricular (PVN) and supraoptic (SON) nuclei and is released via the neurohypophysis into circulation in response to uterine contractions and mammary gland stimulation (8). OT is also released within the PVN and SON (intranuclear release) (28), which is thought to be critical for initiating and coordinating the firing activities of the magnocellular OT neurons responsible for systemic OT release during parturition and lactation (23,27).A number of changes in the OT system have been documented during late gestation: central OT mRNA is increased (7,26,33,39,41), morphological rearrangements of magnocellular nuclei facilitate increased connectivity of soma and dendrites in OT neurons (37), and electrophysiological changes in OT neuronal firing patterns (18) and in active membrane properties (35) are associated with increases in spontaneous bursting. As a likely consequence of these changes, OT concentrations in the neural lobe (13, 22) and systemic OT release (22...

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“…Mast cells could either induce CRH release or some hypothalamic mast cell mediator could independently activate the HPA axis. For instance, histamine and interleukin-6 can stimulate CRH release (Kjaer et al, 1998), and interleukin-6 has been shown to be a CRH-independent activator of the HPA axis (Bethin et al, 2000). Taken together, these results indicate that there are bidirectional actions of CRH on mast cells and such interactions (Rozniecki et al, 1999) could contribute in diseases exacerbated by stress (Theoharides, 2002).…”

Section: Discussionmentioning

confidence: 85%

Corticotropin-Releasing Hormone and Brain Mast Cells Regulate Blood-Brain-Barrier Permeability Induced by Acute Stress

Esposito

Chandler

Kandere

et al. 2002

J Pharmacol Exp Ther

221

133

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Stress activates the hypothalamic-pituitary-adrenal axis through release of corticotropin releasing hormone (CRH), leading to production of glucocorticoids that down-regulate immune responses. Acute stress, however, also has proinflammatory effects that seem to be mediated through the activation of mast cells. Stress and mast cells have been implicated in the pathophysiology of various inflammatory conditions, including some in the central nervous system, such as multiple sclerosis in which disruption of the blood-brain barrier (BBB) precedes clinical symptoms. We previously showed that acute restraint stress increases rat BBB permeability to intravenous 99 Tc gluceptate and that administration of the "mast cell stabilizer" disodium cromoglycate (cromolyn) inhibits this effect. In this study, we show that the CRH-receptor antagonist Antalarmin blocks stress-induced 99 Tc extravasation, whereas site-specific injection of CRH in the paraventricular nucleus (PVN) of the hypothalamus mimics acute stress. This latter effect is blocked by pretreatment of the PVN with cromolyn; moreover, restraint stress cannot disrupt the BBB in the diencephalon and cerebellum of W/W v mast cell-deficient mice. These results demonstrate that CRH and mast cells are involved in regulating BBB permeability and, possibly, brain inflammatory disorders exacerbated by acute stress.

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Neuronal histamine and expression of corticotropin-releasing hormone, vasopressin and oxytocin in the hypothalamus: relative importance of H1 and H2 receptors

Cited by 50 publications

References 37 publications

Histidine decarboxylase deficiency in gene knockout mice elevates male sex steroid production

Histidine decarboxylase deficiency in gene knockout mice elevates male sex steroid production

Differential sensitivity of intranuclear and systemic oxytocin release to central noradrenergic receptor stimulation during mid- and late gestation in rats

Corticotropin-Releasing Hormone and Brain Mast Cells Regulate Blood-Brain-Barrier Permeability Induced by Acute Stress

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