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Acetylcholine

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Lee A Dawson – One of the best experts on this subject based on the ideXlab platform.

  • attenuation of amphetamine induced activity by the non selective muscarinic receptor agonist xanomeline is absent in muscarinic m4 receptor knockout mice and attenuated in muscarinic m1 receptor knockout mice
    European Journal of Pharmacology, 2009
    Co-Authors: Marie L Woolley, Helen J Carter, Jane Gartlon, Jeanette Watson, Lee A Dawson

    Abstract:

    Abstract The muscarinic Acetylcholine receptor (mAChR) agonist, xanomeline, attenuates amphetamine-induced activity in WT mice. This effect is abolished in mice lacking the M4 muscarinic Acetylcholine receptor (M4 mAChR KO) and partially attenuated in mice lacking M1 muscarinic Acetylcholine receptor (M1 mAChR KO). Collectively, these data suggest that the efficacy exhibited by xanomeline in the mouse amphetamine-induced hyperactivity model, is mediated predominantly by M4 muscarinic Acetylcholine receptors, and that M1 muscarinic Acetylcholine receptors may play a more minor role. This supports the hypothesis that activation of M4, and to a lesser extent M1 muscarinic Acetylcholine receptors, may represent a potential target for the treatment of psychosis seen in schizophrenia.

Marie L Woolley – One of the best experts on this subject based on the ideXlab platform.

  • attenuation of amphetamine induced activity by the non selective muscarinic receptor agonist xanomeline is absent in muscarinic m4 receptor knockout mice and attenuated in muscarinic m1 receptor knockout mice
    European Journal of Pharmacology, 2009
    Co-Authors: Marie L Woolley, Helen J Carter, Jane Gartlon, Jeanette Watson, Lee A Dawson

    Abstract:

    Abstract The muscarinic Acetylcholine receptor (mAChR) agonist, xanomeline, attenuates amphetamine-induced activity in WT mice. This effect is abolished in mice lacking the M4 muscarinic Acetylcholine receptor (M4 mAChR KO) and partially attenuated in mice lacking M1 muscarinic Acetylcholine receptor (M1 mAChR KO). Collectively, these data suggest that the efficacy exhibited by xanomeline in the mouse amphetamine-induced hyperactivity model, is mediated predominantly by M4 muscarinic Acetylcholine receptors, and that M1 muscarinic Acetylcholine receptors may play a more minor role. This supports the hypothesis that activation of M4, and to a lesser extent M1 muscarinic Acetylcholine receptors, may represent a potential target for the treatment of psychosis seen in schizophrenia.

Masato Tsutsui – One of the best experts on this subject based on the ideXlab platform.

  • ikarisoside a inhibits Acetylcholine induced catecholamine secretion and synthesis by suppressing nicotinic Acetylcholine receptor ion channels in cultured bovine adrenal medullary cells
    Naunyn-schmiedebergs Archives of Pharmacology, 2015
    Co-Authors: Xiaojia Li, Yumiko Toyohira, Takafumi Horisita, Noriaki Satoh, Keita Takahashi, Han Zhang, Munekazu Iinuma, Yukari Yoshinaga, Susumu Ueno, Masato Tsutsui

    Abstract:

    Ikarisoside A is a natural flavonol glycoside derived from plants of the genus Epimedium, which have been used in Traditional Chinese Medicine as tonics, antirheumatics, and aphrodisiacs. Here, we report the effects of ikarisoside A and three other flavonol glycosides on catecholamine secretion and synthesis in cultured bovine adrenal medullary cells. We found that ikarisoside A (1–100 μM), but not icariin, epimedin C, or epimedoside A, concentration-dependently inhibited the secretion of catecholamines induced by Acetylcholine, a physiological secretagogue and agonist of nicotinic Acetylcholine receptors. Ikarisoside A had little effect on catecholamine secretion induced by veratridine and 56 mM K+. Ikarisoside A (1–100 μM) also inhibited 22Na+ influx and 45Ca2+ influx induced by Acetylcholine in a concentration-dependent manner similar to that of catecholamine secretion. In Xenopus oocytes expressing α3β4 nicotinic Acetylcholine receptors, ikarisoside A (0.1–100 μM) directly inhibited the current evoked by Acetylcholine. It also suppressed 14C-catecholamine synthesis and tyrosine hydroxylase activity induced by Acetylcholine at 1–100 μM and 10–100 μM, respectively. The present findings suggest that ikarisoside A inhibits Acetylcholine-induced catecholamine secretion and synthesis by suppression of nicotinic Acetylcholine receptor-ion channels in bovine adrenal medullary cells.