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Alpha Fluoromethylhistidine

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Zhong Chen – One of the best experts on this subject based on the ideXlab platform.

  • apomorphine induced turning behavior in 6 hydroxydopamine lesioned rats is increased by histidine and decreased by histidine decarboxylase histamine h1 and h2 receptor antagonists and an h3 receptor agonist
    Pharmacology Biochemistry and Behavior, 2008
    Co-Authors: Chunqing Liu, Zhong Chen, Fuxin Liu, Jianhong Luo

    Abstract:

    The role of histamine and its receptors in basal ganglia neurocircuitry was assessed in apomorphine-induced turning behavior. Rats with unilateral 6-hydroxydopamine lesions of the substantia nigra pars compacta and medial forebrain bundle were administered histaminergic agents, and apomorphine-induced turning behavior was tested on Days 7 and 14 post-lesion. Compared with saline-treated rats, histidine (500 mg/kg, i.p.), a precursor of histamine, increased turning behavior (p<0.05), while AlphaFluoromethylhistidine (Alpha-FMH, 25 microg, i.c.v.), an irreversible inhibitor of histidine decarboxylase, decreased turning behavior (p<0.05) but only on Day 14 post-lesion. Both the histamine H(1) receptor antagonist pyrilamine (10 and 50 microg, i.c.v.) and the H(2) receptor antagonist cimetidine (10 and 50 microg, i.c.v.) significantly decreased turning behavior on Days 7 and 14 post-lesion. The histamine H(3) receptor agonist immepip (10 microg, i.c.v.) decreased turning behavior (p<0.05) on Day 14 post-lesion. The present findings indicate the complex interactions of histamine on basal ganglia function.

  • Carnosine Protects Against Aβ42-induced Neurotoxicity in Differentiated Rat PC12 Cells
    Cellular and molecular neurobiology, 2007
    Co-Authors: Haibin Dai, Yan-ying Fan, Yao Shen, Weiping Zhang, Zhong Chen

    Abstract:

    (1) The present study was designed to investigate whether histamine is involved in the protective effect of carnosine on Abeta42-induced impairment in differentiated PC12 cells. (2) PC12 cells were exposed to Abeta42 (5 muM) for 24 h after carnosine (5 mM) applied for 18 h. Histamine receptor antagonists (diphenhydramine, zolantidine, thioperamide, clobenpropit) or histidine decarboxylase inhibitor (AlphaFluoromethylhistidine) were added 15 min before carnosine. Cell viability, glutamate release or cell surface expression of NMDA receptor was examined. (3) Abeta42 caused a concentration-dependent reduction of viability in PC12 cells and pretreatment with carnosine ameliorated this impairment. This amelioration was reversed by the H(3) receptor antagonists thioperamide and clobenpropit, but not by either the H(1) receptor antagonist diphenhydramine or the H(2) receptor antagonist zolantidine. Further, AlphaFluoromethylhistidine, an irreversible inhibitor of histidine decarboxylase, also had no effect. In the presence of Abeta42, carnosine significantly decreased glutamate release and carnosine increased the surface expression of NMDA receptor. (4) These results indicate that the mechanism by which carnosine attenuates Abeta42-induced neurotoxicity is independent of the carnosine-histidine-histamine pathway, but may act through regulation of glutamate release and NMDA receptor trafficking.

  • Neuroprotective effect of carnosine on necrotic cell death in PC12 cells
    Neuroscience letters, 2006
    Co-Authors: Yao Shen, Yan-ying Fan, Haibin Dai, Zhong Chen

    Abstract:

    The nervous tissue of many vertebrates, including humans, can synthesize beta-alanyl-L-histidine (carnosine). The biological functions of carnosine are still open to question, although several theories supported by strong experimental data have been proposed. The objective of this study was to examine the effects of carnosine on neurotoxicity in differentiated rat pheochromocytoma (PC12) cells. Neurotoxicity was induced by N-methyl-D-aspartate (NMDA), which caused time- and concentration-dependent cell death as measured by MTT and LDH assays. Pretreatment with carnosine significantly prevented the neurotoxicity in a concentration-dependent manner. The protective effect of carnosine was antagonized by the H1 receptor antagonist pyrilamine, but not by the H2 receptor antagonist cimetidine. In addition, AlphaFluoromethylhistidine, a histidine decarboxylase inhibitor, slightly reversed the protective action of carnosine. These results indicate that carnosine can effectively protect against NMDA-induced necrosis in PC12 cells, and its protection may in part be due to the activation of the postsynaptic histamine H1 receptor. The study suggests that carnosine may be an endogenous protective factor and calls for its further study as a new anti-excitotoxic agent.

Kazuhiko Yanai – One of the best experts on this subject based on the ideXlab platform.

  • Effect of the histamine H3-antagonist clobenpropit on spatial memory deficits induced by MK-801 as evaluated by radial maze in Sprague-Dawley rats.
    Behavioural brain research, 2004
    Co-Authors: Yuwen Huang, Zhong Chen, Lisan Zhang, Hai-qing Shen, Henk Timmerman, Rob Leurs, Kazuhiko Yanai

    Abstract:

    This study was performed to investigate whether or not the histamine H3-antagonist clobenpropit can ameliorate spatial memory deficits induced by MK-801 (0.3 microg per site) as evaluated by an eight-arm radial maze task of rats. A bilateral intrahippocampal (i.h.) injection of clobenpropit (5, 10 microg per site, dose-dependent) markedly improved the working and reference memory deficits induced by MK-801. Its ameliorating effect was potentiated by histidine, but completely antagonized by immepip (2.5 microg per site), a selective H3-agonist. AlphaFluoromethylhistidine (FMH, 25 microg per site), a selective histidine decarboxylase inhibitor prevented the ameliorating effect of clobenpropit on the working memory deficits induced by MK-801. In addition, the H(1-antagonist pyrilamine, but not the H2-antagonist cimetidine, also inhibited the procognitive effects of clobenpropit. Both FMH and pyrilamine did not significantly modulate the effect of clobenpropit on reference memory. Therefore, the results of this study suggest that the procognitive effects of clobenpropit in MK-801-induced working memory deficits is mediated by increasing endogenous histamine release. In addition, the ameliorating effect of clobenpropit on reference memory might be due to the increased release of neurotransmitters other than histamine.

  • The effect of dopamine D1 receptor stimulation on the up-regulation of histamine H3-receptors following destruction of the ascending dopaminergic neurones
    British journal of pharmacology, 1996
    Co-Authors: Jong Hoon Ryu, Kazuhiko Yanai, Xiao-lan Zhao, Takehiko Watanabe

    Abstract:

    1. The binding of [3H]-(R)Alpha-methylhistamine and [3H]-N Alpha-methylhistamine to histamine H3-receptors, [3H]-SCH23390 to dopamine D1-receptors, and [3H]-YM09151-2 to dopamine D2-receptors was investigated by quantitative receptor autoradiography in the rat brain following 6-hydroxydopamine injection into the substantia nigra. 2. The levels of [3H]-(R)Alpha-methylhistamine binding sites in the denervated striatum and substantia nigra were significantly higher than those in the contralateral side from 1 week to 12 weeks after nigral lesions. The H3-receptor binding was maximal at 3 weeks after nigral lesions and maintained until 12 weeks. 3. The increased number of histamine H3-receptors was decreased to the level of the contralateral side by chronic treatment with a selective dopamine D1 agonist, SKF38393, but not modified by a selective dopamine D2 agonist, quinpirole. 4. Dopamine D1- and D2-receptors in the striatum were similarly up-regulated after unilateral nigral lesion. On the other hand, the number of dopamine D2-receptors in the substantia nigra was markedly decreased after administration of 6-hydroxydopamine. 5. The treatment with (S)AlphaFluoromethylhistidine increased the H3-receptor binding in both the ipsilateral and contralateral sides. As a result, the magnitude of the ratio of the H3-receptor binding between ipsilateral and contralateral sides was partially attenuated by treatment with (S)-AlphaFluoromethylhistidine. 6. These results strongly suggest that the expression of histamine H3-receptors in the striatum and substantia nigra is influenced through D1-receptors by tonic nigrostriatal dopaminergic inputs.

  • Histamine depletion in brain caused by treatment with (S) α-Fluoromethylhistidine enhances ischemic damage of gerbil hippocampal CA2 neurons
    Brain research, 1994
    Co-Authors: Koreaki Sugimoto, Koji Abe, T. H. Lee, Eiko Sakurai, Kazuhiko Yanai, Kyuya Kogure, Yasuto Itoyama, Takehiko Watanabe

    Abstract:

    The effect of (S)AlphaFluoromethylhistidine (FMH), a specific inhibitor of histamine synthesis from histidine, on ischemic damage was examined in gerbil brain after forebrain ischemia. Two h after subcutaneous FMH injection, the histamine content of the brain was significantly reduced. Neuronal loss in the CA2 region of the hippocampus 7 days after 3 min ischemia was enhanced by treatment with FMH. These results indicate that depletion of brain histamine aggravates neuronal death of hippocampal CA2 neurons after 3 min ischemia.

Takehiko Watanabe – One of the best experts on this subject based on the ideXlab platform.

  • Brain Histaminergic System in Mast Cell‐Deficient (Ws/Ws) Rats: Histamine Content, Histidine Decarboxylase Activity, and Effects of (S)α‐Fluoromethylhistidine
    Journal of neurochemistry, 2002
    Co-Authors: K. Sugimoto, Eiko Sakurai, Kazutaka Maeyama, M. Khorshed Alam, Hitoshi Onoue, Tsutomu Kasugai, Yukihiko Kitamura, Takehiko Watanabe

    Abstract:

    The mast cell-deficient [Ws/Ws (White spotting in the skin)] rat was investigated with regard to the origin of histamine in the brain. No mast cells were detected in the pia mater and the perivascular region of the thalamus of Ws/Ws rats by Alcian Blue staining. The histamine contents and histidine decarboxylase (HDC) activities of various brain regions of Ws/Ws rats were similar to those of +/+ rats except the histamine contents of the cerebral cortex and cerebellum. As the cerebral cortex and cerebellum have meninges that are difficult to remove completely, the histamine contents of these two regions may be different between Ws/Ws and +/+ rats. We assume that the histamine content of whole brain with meninges in Ws/Ws rats is < 60% of that in +/+ rats. So we conclude that approximately half of the histamine content of rat brain is derived from mast cells. Next, the effects of (S) AlphaFluoromethylhistidine (FMH), a specific inhibitor of HDC, on the histamine contents and HDC activities of various regions of the brain were examined in Ws/Ws rats. In the whole brain of Ws/Ws rats, 51 and 37% of the histamine content of the control group remained 2 and 6 h, respectively, after FMH administration (100 mg/kg of body weight). Therefore, we suggest that there might be other histamine pools including histaminergic neurons in rat brain.

  • The effect of dopamine D1 receptor stimulation on the up-regulation of histamine H3-receptors following destruction of the ascending dopaminergic neurones
    British journal of pharmacology, 1996
    Co-Authors: Jong Hoon Ryu, Kazuhiko Yanai, Xiao-lan Zhao, Takehiko Watanabe

    Abstract:

    1. The binding of [3H]-(R)Alpha-methylhistamine and [3H]-N Alpha-methylhistamine to histamine H3-receptors, [3H]-SCH23390 to dopamine D1-receptors, and [3H]-YM09151-2 to dopamine D2-receptors was investigated by quantitative receptor autoradiography in the rat brain following 6-hydroxydopamine injection into the substantia nigra. 2. The levels of [3H]-(R)Alpha-methylhistamine binding sites in the denervated striatum and substantia nigra were significantly higher than those in the contralateral side from 1 week to 12 weeks after nigral lesions. The H3-receptor binding was maximal at 3 weeks after nigral lesions and maintained until 12 weeks. 3. The increased number of histamine H3-receptors was decreased to the level of the contralateral side by chronic treatment with a selective dopamine D1 agonist, SKF38393, but not modified by a selective dopamine D2 agonist, quinpirole. 4. Dopamine D1- and D2-receptors in the striatum were similarly up-regulated after unilateral nigral lesion. On the other hand, the number of dopamine D2-receptors in the substantia nigra was markedly decreased after administration of 6-hydroxydopamine. 5. The treatment with (S)AlphaFluoromethylhistidine increased the H3-receptor binding in both the ipsilateral and contralateral sides. As a result, the magnitude of the ratio of the H3-receptor binding between ipsilateral and contralateral sides was partially attenuated by treatment with (S)-AlphaFluoromethylhistidine. 6. These results strongly suggest that the expression of histamine H3-receptors in the striatum and substantia nigra is influenced through D1-receptors by tonic nigrostriatal dopaminergic inputs.

  • Histamine depletion in brain caused by treatment with (S) α-Fluoromethylhistidine enhances ischemic damage of gerbil hippocampal CA2 neurons
    Brain research, 1994
    Co-Authors: Koreaki Sugimoto, Koji Abe, T. H. Lee, Eiko Sakurai, Kazuhiko Yanai, Kyuya Kogure, Yasuto Itoyama, Takehiko Watanabe

    Abstract:

    The effect of (S)AlphaFluoromethylhistidine (FMH), a specific inhibitor of histamine synthesis from histidine, on ischemic damage was examined in gerbil brain after forebrain ischemia. Two h after subcutaneous FMH injection, the histamine content of the brain was significantly reduced. Neuronal loss in the CA2 region of the hippocampus 7 days after 3 min ischemia was enhanced by treatment with FMH. These results indicate that depletion of brain histamine aggravates neuronal death of hippocampal CA2 neurons after 3 min ischemia.