Disease relevance of Hrh1

• We report that the contribution of Bphs/Hrh1 to the overall genetic control of responsiveness to PTX is restricted to susceptibility to histamine hypersensitivity and enhancement of antigen-specific delayed-type hypersensitivity responses [1].
• Analysis of the role of Bphs/Hrh1 in the genetic control of responsiveness to pertussis toxin [1].
• Bphs/Hrh1 also did not significantly influence susceptibility to the lethal effects, the leukocytosis response, disruption of glucose regulation, and histamine-independent increases in vascular permeability associated with in vivo intoxication [1].
• Locus controlling Bordetella pertussis-induced histamine sensitization (Bphs), an autoimmune disease-susceptibility gene, maps distal to T-cell receptor beta-chain gene on mouse chromosome 6 [2].
• Involvement of hypothalamic histamine H1 receptor in the regulation of feeding rhythm and obesity [3].

Psychiatry related information on Hrh1

• The opioid agonist-antagonist pentazocine (1-30 mg/kg) and the partial agonist buprenorphine (0.05-0.25 mg/kg) were tested, alone or in combination with the histamine H1-receptor antagonist tripelennamine (1, 2.5, 5 or 10 mg/kg), on locomotor activity in mice of the CD-1 strain [4].
• We have shown that morphine has an anticonvulsive effect against maximal electroconvulsive shock (MES) in mice, and this effect is antagonized by histamine H1-receptor antagonists [5].

High impact information on Hrh1

• Histamine H1 receptor-mediated guanosine 3',5'-monophosphate formation by cultured mouse neuroblastoma cells [6].
• We report here the mapping of the Bphs locus to mouse chromosome 6, telomeric of Tcrb and centromeric of Prp (D6Nds8) [2].
• One such agent is histamine, and the response to PTX, as measured by hypersensitivity following vasoactive amine challenge, is genetically controlled by the Bphs locus [2].
• Instead, we have found that muscarinic or histamine H1 receptor stimulation elicits the release of arachidonic acid through a quinacrine-sensitive mechanism, possibly phospholipase A2 [7].
• A histamine H1 receptor agonist [2-(2-pyridyl)-ethylamine dihydrochloride] had a propensity to activate contrasuppression, whereas an H2 receptor agonist (dimaprit) tended to activate suppressor cells [8].

Chemical compound and disease context of Hrh1

• These results suggest that diphenhydramine, a histamine H1 receptor antagonist, reduced the formation of intimal hyperplasia, at least in part due to inhibition of cell proliferation [9].
• Desensitization of histamine H1 receptor-mediated cyclic GMP formation in mouse neuroblastoma cells [10].
• Three histamine H1-receptor antagonists, chlorpheniramine, diphenhydramine and tripelennamine, were tested alone or in combination with morphine, amphetamine and scopolamine on locomotor activity in mice [11].
• The chronic contact hypersensitivity induced by repeated application of oxazolone was treated with olopatadine and other histamine H1 receptor antagonists at the effective doses on histamine-induced paw edema in mice [12].
• Fexofenadine, a histamine H1-receptor antagonist, is approved for the treatment of pruritus associated with atopic dermatitis [13].

Biological context of Hrh1

• Histamine neurons are widely distributed in the brain and suppress food intake through the histamine H1 receptor (H1-R) in the hypothalamus [14].
• Bphs controls Bordetella pertussis toxin (PTX)-induced vasoactive amine sensitization elicited by histamine (VAASH) and has an established role in autoimmunity [15].
• Chemical genetic identification of the histamine H1 receptor as a stimulator of insulin-induced adipogenesis [16].
• 1. 2-Chloroadenosine stimulated adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation and potentiated (guinea-pig) or inhibited (mouse) the histamine H1-receptor-stimulated hydrolysis of inositol phospholipids in slices of guinea-pig and mouse cerebral cortex [17].
• All the synthesized compounds were screened for histamine H1-receptor antagonistic activity by the in vitro method of inhibition of the isotonic contraction induced by histamine on isolated guinea pig ileum using cetirizine as a standard drug [18].

Anatomical context of Hrh1

• Thus, natural alleles of Hrh1 control both the autoimmune T cell and vascular responses regulated by histamine after PTX sensitization [15].
• This effect was antagonized by BP 2.94 (10 mg/kg, i.p.), a prodrug of (R)-alpha-methylhistamine (histamine H3-receptor agonist), and by ketotifen (4 mg/kg, i.p.), a histamine H1-receptor antagonist, both penetrating the blood-brain barrier [19].
• When bone marrow cells were treated with a histamine H1 receptor antagonist prior to histamine treatment, low concentrations of histamine also triggered the entrance of CFU-s into the DNA synthetic phase [20].
• Histamine H1 receptor is expressed in 3T3-L1 cells, and its knockdown by small interfering RNA impaired the insulin-induced adipogenic differentiation [16].
• However, the employment of a polymerase chain reaction (PCR) technique for the detection of mRNA for histamine H1 receptor identified receptor-specific message in isolated cerebrovascular endothelium from both strains of mice [21].

Associations of Hrh1 with chemical compounds

• The histamine H1 receptor agonist 2-pyridylethylamine induced sneezing and nasal rubbing in a dose-dependent-manner in wild-type mice, but no such increase was found in histamine H1 receptor-deficient mice [22].
• Histamine H1 receptor antagonists such as chlorpheniramine and epinastine significantly inhibited nasal allergic symptoms caused by histamine, but the histamine H2 receptor antagonists cimetidine and famotidine showed no effect [22].
• The histamine H1 receptor antagonists diphenhydramine and tripelennamine accelerated the recovery [23].
• It is concluded that in the heart, hormones which increase cAMP and cytosolic Ca2+, such as beta-adrenergic agonists and prostaglandin E1, and/or stimulate the turnover of inositol phospholipids, such as alpha-adrenergic agonists and histamine H1-receptor agonists, regulate c-fos gene expression [24].
• The histamine-induced expression of the c-fos gene was blocked by the histamine H1-receptor antagonist pyrilamine but not by H2-receptor antagonists ranitidine and cimetidine [24].

Physical interactions of Hrh1

• Histamine H1 receptor binding sites in mouse uterine horns [25].

Other interactions of Hrh1

• The antinociceptive effects of i.c.v. orexin A were greater in histamine H1 receptor or H2 receptor knockout mice than in the wild-type mice in all four assays of pain [26].
• Development of amygdaloid kindling in histidine decarboxylase-deficient and histamine H1 receptor-deficient mice [27].
• CD4+ T-cells from histamine H1 receptor (H1R)-deficient (H1RKO) mice produce significantly less interferon-gamma and more interleukin (IL)-4 in in vitro recall assays compared to wild-type controls [28].
• Physical mapping of the autoimmune disease susceptibility locus, Bphs: co-localization with a cluster of genes from the TNF receptor superfamily on mouse chromosome 6 [29].
• Targeted disruption of histamine H1-receptor attenuates regulatory effects of leptin on feeding, adiposity, and UCP family in mice [14].

Analytical, diagnostic and therapeutic context of Hrh1

• We report here the molecular cloning of a mouse histamine H1 receptor gene [30].
• 1. Effects of substances which are able to alter brain histamine levels and two histamine H1 receptor agonists were investigated in mice by means of an animal model of depression, the forced swim test [31].
• The histamine H-1 receptor antagonist, pyrilamine (N-((4-methoxyphenyl)methyl)-N',N'-dimethyl-N-2-pyridinyl-1,2-ethaned i ami ne) was labeled with carbon-11 by N-alkylation of desmethylpyrilamine with [11C]iodomethane, and purified by preparative high performance liquid chromatography [32].

References