Articles: histamine.
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In inflamed tissues, extracellular pH decreases and acidosis is an important source of pain. Histamine is released from mast cells under inflammatory conditions and evokes the pain sensation in vivo, but the cellular mechanism of histamine-induced pain has not been well understood. In the present study, we examined the effects of histamine on [Ca(2+)](i) and membrane potential responses to acid in isolated mouse dorsal root ganglion (DRG) neurons. ⋯ A lipoxygenase inhibitor and protein kinase A inhibitor did not affect the potentiating effects of histamine. Carrageenan and complete Freund's adjuvant produced inflammatory hyperalgesia, but these inflammatory conditions did not change the potentiating effects of histamine in DRG neurons. The present results suggest that histamine sensitizes acid-induced responses through TRPV1 activation via H1R coupled with PLC/PKC pathways, the action of which may be involved in the generation of inflammatory pain.
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Brain neuronal histamine, through its receptors, is involved in central pain perception. In the present study, the effect of microinjection of histamine, mepyramine (a histamine H(1) receptor antagonist) and ranitidine (a histamine H(2) receptor antagonist) into the dorsal hippocampus was investigated on a model of orofacial pain in rats. Orofacial pain was induced by subcutaneous injection of formalin (1%, 50 microl) in the upper lip in rats, and the time spent of face rubbing was measured in 3-min blocks for 45 min. ⋯ Pretreatments with mepyramine and ranitidine at a same dose of 4 microg prevented histamine (1 microg)-induced antinociception. These results indicate that the activation of brain neuronal histamine at the levels of the hippocampus may produce antinociception. Hippocampal histamine-induced antinociception may be mediated thorough its H(1) and H(2) receptors.
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Recent research has proposed a pathway in which sensory neurons expressing the capsaicin activated ion channel TRPV1 are required for histamine-induced itch and subsequent scratching behavior. We examined histamine-induced itch in the African naked mole-rat (Heterocephalus glaber) and found that although naked mole-rats display innate scratching behavior, histamine was unable to evoke increased scratching as is observed in most mouse strains. Using calcium imaging, we examined the histamine sensitivity of naked mole-rat dorsal root ganglia (DRG) neurons and identified a population of small diameter neurons activated by histamine, the majority of which are also capsaicin-sensitive. ⋯ Our data therefore support a model in which TRPV1-expressing sensory neurons are important for histamine-induced itch. In addition, we demonstrate a requirement for active, SP-induced post-synaptic drive to enable histamine sensitive afferents to drive itch-related behavior in the naked mole-rat. These results illustrate that it is altered dorsal horn connectivity of nociceptors that underlies the lack of itch and pain-related behavior in the naked mole-rat.
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The tuberomammillary histaminergic neurons are involved in the sedative component of anesthetic action. The nucleus basalis magnocellularis (NBM) in the basal forebrain receives dense excitatory innervation from the tuberomammillary nucleus and is recognized as an important site of sleep-wake regulation. This study investigated whether NBM administration of histaminergic drugs may modulate arousal/emergence from isoflurane anesthesia. ⋯ Histamine activation of H1 receptors in the NBM induces electroencephalographic arousal and facilitates emergence from isoflurane anesthesia. The basal forebrain histaminergic pathway appears to play a role in modulating arousal/emergence from anesthesia.
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Clinical Trial
Similar itch and nociceptive sensations evoked by punctate cutaneous application of capsaicin, histamine and cowhage.
Itch evoked by cowhage or histamine is reduced or blocked by capsaicin desensitization, suggesting that pruriceptive neurons are capsaicin-sensitive. Topical capsaicin can evoke both nociceptive sensations and itch, whereas intradermal injection of capsaicin evokes only burning pain. To dissociate the pruritic and nociceptive sensory effects caused by the chemical activation of sensory neurons, chemicals were applied in a punctiform manner to the skin of the forearm using individual, heat-inactivated cowhage spicules treated with various concentrations of capsaicin (1-200 mg/ml) or histamine (0.01-100 mg/ml). ⋯ Each type of spicule also produced comparable areas of dysesthesias (enhanced mechanically evoked itch or pain) and/or skin reactions (wheal and/or flare) in surrounding skin, though inconsistently. The incidence of flare was greater in response to histamine than to capsaicin or cowhage. These results suggest the possibility that capsaicin, histamine and cowhage activate common peripheral or central neural mechanisms that mediate pruritic sensations and associated dysesthesias.