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Friday, 13 December 2013

The Effects of Hormone Histamine (3)

Histamine, found within granules of basophils and mast cells (>90% of body stores) is a biogenic amine and an organic nitrogen compound that occurs to various degrees in many foods such as cherries to about 0.17-13.46 ng/g, bananas and grapes, rice and cereals, herbs, olive oil, wine, beer, etc.. In healthy persons, dietary histamine can be rapidly detoxified by amine oxidases, whereas persons with low amine oxidase activity are at risk of histamine toxicity(a). the hormone, as a neurotransmitter is involved in regulating physiological function in the gut and immune response to foreign pathogens.
19. Histamine and IgE-mediated diseases
Skin tests are used in addition to a directed history and physical exam to exclude or confirm IgE-mediated diseases such as allergic rhinitis, asthma, and anaphylaxis to aeroallergens, foods, insect venoms, and certain drugs. Prick testing involves introducing a needle into the upper layers of the skin through a drop of allergen extract and gently lifting the epidermis up. Other devices are available for prick testing. Intracutaneous (intradermal) testing involves injecting a small amount of allergen (0.01-0.02 mL) into the dermis. The release of preformed histamine from mast cells causes increased vascular permeability via smooth muscle contraction and development of a wheal; inflammatory mediators initiate a neural reflex causing vasodilatation, leading to erythema (the flare)(19).

20. Role of histamine in motion sickness
In the study to elucidate the role of histamine in motion sickness, researchers at the Faculty of Pharmaceutical Sciences, University of Tokyo, found that shaking the animals for 2 min increased HA contents in telencephalon and diencephalon without significantly changing the t-MH levels. alpha-Fluoromethylhistidine (alpha-FMH), which is presumed to deplete the neuronal HA, tended to raise the HA levels. alpha-FMH slightly alleviated the vomiting response to motion stimulus and suppressed the HA increase in diencephalon caused by shaking. Compound 48/80, which releases HA from mast cells, did not alter the control HA levels, but effectively prevented the motion sickness and completely suppressed the motion-induced rises in HA levels. These results provide further evidence that brain HA plays an important role in the development of motion sickness(20).

21. Histamine and motivation
Brain histamine may affect a variety of different behavioral and physiological functions; however, its role in promoting wakefulness has overshadowed its other important functions. Evidence indicated that brain histamine plays a central role in motivation and emphasize its differential involvement in the appetitive and consummatory phases of motivated behaviors(21).

22. Histamine in addiction and addiction-related behaviors
Research conducted during the past decade demonstrated that the ability of many antihistaminic drugs to potentiate addiction-related behaviors essentially results from non-specific effects and does not constitute a valid argument in support of an inhibitory function of histamine on reward processes. The reviewed findings also indicate that histamine can either stimulate or inhibit the dopamine mesolimbic system through distinct neuronal mechanisms involving different histamine receptors(22).

23. Low cerebrospinal fluid (CSF) histamine levels and  hypersomnia
Researchers at the Akita University School of Medicine confirmed that reduced CSF histamine levels in hypocretin-deficient narcolepsy with cataplexy. Similar degrees of reduction were also observed in hypocretin non-deficient narcolepsy and in idiopathic hypersomnia, while those in OSAS (non central nervous system hypersomnia) were not altered. The decrease in histamine in these subjects were more specifically observed in non-medicated subjects, suggesting CSF histamine is a biomarker reflecting the degree of hypersomnia of central origin(23)

24. Histamine and stimulate gastric acid secretion
Ghrelin, a novel growth hormone-releasing peptide, is present in the rat and human stomach and is known to stimulate acid secretion and stomach motility. In the stidy to  to elucidate the role of histamine in ghrelin-induced acid secretion in rat stomach. Intravenous administration of ghrelin at 0.8 to 20 microg/kg dose dependently increased gastric acid secretion, as measured by the gastric lumen perfusion method. The maximum response was almost equal to that of gastrin (20 microg/kg), showed that ghrelin increased histidine decarboxylase (HDC) messenger RNA (mRNA) levels, as measured by real-time reverse transcription-polymerase chain reaction using LightCycler. The action of ghrelin on HDC mRNA was abolished by vagotomy. Ghrelin did not affect histamine release from isolated vascularly perfused rat stomach. Taken together, these results suggest that ghrelin stimulates gastric acid secretion via a mechanism involving activation of vagal efferent nerve and histamine release from gastric enterochromaffin-like cells(24).

25. Histamine and neurotransmitter release
In the study to investigate the effect of histamine-3 (H(3)) receptors, expressed in the tuberomammillary nucleus (TMN) of the hypothalamus and in the prefrontal cortex (PFC), on histamine neurotransmission in the rat brain, showed that systemic administration of the selective H(3)-agonist, immepip, decreases, and the reverse H(3) /H(4)-agonist, thioperamide, increases the firing activity of histamine neurons in the TMN and the release of histamine in TMN and PFC. Local perfusion of immepip into the TMN increased, and thioperamide decreased, histamine levels in the TMN but not in the PFC. Local perfusion of immepip into the PFC, however, decreased extracellular histamine levels in both TMN and PFC. It can be concluded that brain H(3) receptors, and especially those expressed in the PFC, play an important role in the autoregulation of histamine neurotransmission(25)

26. Histamine and noradrenaline and acetylcholine
In the study the effects of different histamine concentrations (1 X 10(-6) to 1 X 10(-4)M) on the contractile effects of noradrenaline and acetylcholine on isolated smooth-muscle preparations from rats, showed that histamine increases 2.6 to 16.2 times the noradrenaline concentrations needed for inducing 50 per cent of the maximum contractile response of the anococcygeal muscle. The interaction between noradrenaline and histamine on this smooth-muscle preparation is not competitive. Histamine in the concentrations applied does not influence the contractile effects of noradrenaline on vas deferens and of acetylcholine on tracheal smooth-muscle preparation. In rat anococcygeal muscle histamine most probably influences the contractile effects of noradrenaline and acetylcholine through allosteric interaction with their receptors(26).

27. The role of histamine H4 receptor in immune and inflammatory disorders
In the study the efficacy of a number of H4 receptor ligands has been evaluated in in vivo and in vitro animal models of disease and in human biological samples, showed that  the available data strongly point to the H4 receptor as a novel target for the pharmacological modulation of histamine-transferred immune signals and offer an optimistic perspective for the therapeutic exploitation of this promising new drug target in inflammatory disorders(27).

28. The role of histamine H1 and H4 receptors in allergic inflammation
In the study to the effect of histamine  in allergic inflammatory conditions, showed that histamine indeed has roles in inflammation and immune function modulation in such diseases. In particular, the discovery of a fourth histamine receptor (H4) and its expression on numerous immune and inflammatory cells has prompted a re-evaluation of the actions of histamine, suggesting a new potential for H4-receptor antagonists and a possible synergy between H1 and H4-receptor antagonists in targeting various inflammatory conditions(28).

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Sources
(a) http://www.ncbi.nlm.nih.gov/pubmed/17490952
(19) http://www.ncbi.nlm.nih.gov/pubmed/22794675
(20) http://www.ncbi.nlm.nih.gov/pubmed/1741719 
(21) http://www.ncbi.nlm.nih.gov/pubmed/22783171
(22) http://www.ncbi.nlm.nih.gov/pubmed/20638439 
(23) http://www.ncbi.nlm.nih.gov/pubmed/19238805
(24) http://www.ncbi.nlm.nih.gov/pubmed/16838121 
(25) http://www.ncbi.nlm.nih.gov/pubmed/22050612
(26) http://www.ncbi.nlm.nih.gov/pubmed/7315388 
(27) http://www.ncbi.nlm.nih.gov/pubmed/19309354
(28) http://www.ncbi.nlm.nih.gov/pubmed/18172439