triprolidine and clobenpropit

triprolidine has been researched along with clobenpropit* in 4 studies

Other Studies

4 other study(ies) available for triprolidine and clobenpropit

ArticleYear
Histamine excites neonatal rat sympathetic preganglionic neurons in vitro via activation of H1 receptors.
    Journal of neurophysiology, 2006, Volume: 95, Issue:4

    The role of histamine in regulating excitability of sympathetic preganglionic neurons (SPNs) and the expression of histamine receptor mRNA in SPNs was investigated using whole-cell patch-clamp electrophysiological recording techniques combined with single-cell reverse transcriptase polymerase chain reaction (RT-PCR) in transverse neonatal rat spinal cord slices. Bath application of histamine (100 microM) or the H1 receptor agonist histamine trifluoromethyl toluidide dimaleate (HTMT; 10 microM) induced membrane depolarization associated with a decrease in membrane conductance in the majority (70%) of SPNs tested, via activation of postsynaptic H1 receptors negatively coupled to one or more unidentified K+ conductances. Histamine and HTMT application also induced or increased the amplitude and/or frequency of membrane potential oscillations in electrotonically coupled SPNs. The H2 receptor agonist dimaprit (10 microM) or the H3 receptor agonist imetit (100 nM) were without significant effect on the membrane properties of SPNs. Histamine responses were sensitive to the H1 receptor antagonist triprolidine (10 microM) and the nonselective potassium channel blocker barium (1 mM) but were unaffected by the H2 receptor antagonist tiotidine (10 microM) and the H3 receptor antagonist, clobenpropit (5 microM). Single cell RT-PCR revealed mRNA expression for H1 receptors in 75% of SPNs tested, with no expression of mRNA for H2, H3, or H4 receptors. These data represent the first demonstration of H1 receptor expression in SPNs and suggest that histamine acts to regulate excitability of these neurons via a direct postsynaptic effect on H1 receptors.

    Topics: Action Potentials; Animals; Animals, Newborn; Autonomic Fibers, Preganglionic; Barium; Dimaprit; Female; Ganglia, Sympathetic; Histamine; Histamine Agonists; Histamine H1 Antagonists; Imidazoles; In Vitro Techniques; Male; Membrane Potentials; Neurons; Patch-Clamp Techniques; Potassium; Rats; Rats, Inbred WKY; Receptors, Histamine H1; Receptors, Histamine H2; Receptors, Histamine H3; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Thiourea; Triprolidine

2006
Histaminergic neurons protect the developing hippocampus from kainic acid-induced neuronal damage in an organotypic coculture system.
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006, Jan-25, Volume: 26, Issue:4

    The central histaminergic neuron system inhibits epileptic seizures, which is suggested to occur mainly through histamine 1 (H1) and histamine 3 (H3) receptors. However, the importance of histaminergic neurons in seizure-induced cell damage is poorly known. In this study, we used an organotypic coculture system and confocal microscopy to examine whether histaminergic neurons, which were verified by immunohistochemistry, have any protective effect on kainic acid (KA)-induced neuronal damage in the developing hippocampus. Fluoro-Jade B, a specific marker for degenerating neurons, indicated that, after the 12 h KA (5 microM) treatment, neuronal damage was significantly attenuated in the hippocampus cultured together with the posterior hypothalamic slice containing histaminergic neurons [HI plus HY (POST)] when compared with the hippocampus cultured alone (HI) or with the anterior hypothalamus devoid of histaminergic neurons. Moreover, alpha-fluoromethylhistidine, an inhibitor of histamine synthesis, eliminated the neuroprotective effect in KA-treated HI plus HY (POST), and extracellularly applied histamine (1 nM to 100 microM) significantly attenuated neuronal damage only at 1 nM concentration in HI. After the 6 h KA treatment, spontaneous electrical activity registered in the CA1 subregion contained significantly less burst activity in HI plus HY (POST) than in HI. Finally, in KA-treated slices, the H3 receptor antagonist thioperamide enhanced the neuroprotective effect of histaminergic neurons, whereas the H1 receptor antagonists triprolidine and mepyramine dose-dependently decreased the neuroprotection in HI plus HY (POST). Our results suggest that histaminergic neurons protect the developing hippocampus from KA-induced neuronal damage, with regulation of neuronal survival being at least partly mediated through H1 and H3 receptors.

    Topics: Animals; Cell Death; Cells, Cultured; Coculture Techniques; Convulsants; Hippocampus; Histamine; Histamine Antagonists; Histamine H1 Antagonists; Hypothalamus, Anterior; Hypothalamus, Posterior; Imidazoles; Kainic Acid; Methylhistidines; Microscopy, Confocal; Neurons; Neuroprotective Agents; Organ Culture Techniques; Piperidines; Pyrilamine; Rats; Rats, Sprague-Dawley; Receptors, Histamine H1; Receptors, Histamine H3; Thiourea; Triprolidine

2006
Increase of acetylcholine release from cortex of freely moving rats by administration of histamine into the nucleus basalis magnocellularis.
    Inflammation research : official journal of the European Histamine Research Society ... [et al.], 1998, Volume: 47 Suppl 1

    Topics: Acetylcholine; Animals; Cerebral Cortex; Cimetidine; Electroencephalography; Histamine; Histamine H1 Antagonists; Histamine H2 Antagonists; Imidazoles; Male; Neurons; Rats; Rats, Wistar; Substantia Innominata; Telencephalon; Thiourea; Triprolidine

1998
Histamine inhibits the production of interleukin-12 through interaction with H2 receptors.
    The Journal of clinical investigation, 1998, Nov-15, Volume: 102, Issue:10

    IL-12 is essential for T helper 1 (Th1) development and inhibits the induction of Th2 responses. Atopic diseases, which are characterized by Th2 responses, are associated with the overproduction of histamine. Here we present evidence that histamine, at physiological concentrations, strongly inhibits human IL-12 p40 and p70 mRNA and protein production by human monocytes. The use of specific histamine receptor antagonists reveals that this inhibition is mediated via the H2 receptor and induction of intracellular cAMP. The inhibition of IL-12 production is independent of IL-10 and IFN-gamma. The observation that histamine strongly reduces the production of the Th1-inducing cytokine IL-12 implies a positive feedback mechanism for the development of Th2 responses in atopic patients.

    Topics: Dinoprostone; Histamine; Histamine Agonists; Histamine Antagonists; Histamine H2 Antagonists; Humans; Imidazoles; Interleukin-12; Interleukins; Monocytes; Ranitidine; Receptors, Histamine H2; RNA, Messenger; Thiourea; Triprolidine

1998