Effects of (1R,9S)-[beta]-Hydrastine on Intracellular Calcium Concentration in PC12 Cells
(1R,9S)-β-Hydrastine (BHS) decreases the basal intracellular Ca2+ concentration ([Ca2+]i) in PC12 cells.5) This study examined the effects of (1R,9S)-BHS on [Ca2+]i in PC12 cells. (1R,9S)-BHS at 10--100 μM in combination with a high extracellular K+ level (56 mM) inhibited the release of dopamine in...
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Published in | Biological & pharmaceutical bulletin Vol. 30; no. 8; p. 1547 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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Tokyo
Japan Science and Technology Agency
01.08.2007
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Abstract | (1R,9S)-β-Hydrastine (BHS) decreases the basal intracellular Ca2+ concentration ([Ca2+]i) in PC12 cells.5) This study examined the effects of (1R,9S)-BHS on [Ca2+]i in PC12 cells. (1R,9S)-BHS at 10--100 μM in combination with a high extracellular K+ level (56 mM) inhibited the release of dopamine in a concentration-dependent manner with an IC50 value of 66.5 μM. BHS at 100 μM inhibited the sustained increase in [Ca2+]i induced by a high K+ level (56 mM), and had an inhibitory effect on the 2 μM nifedipine-induced blockage of the K+-stimulated sustained increase in [Ca2+]i. In addition, (1R,9S)-BHS at 100 μM prevented the rapid and sustained increase in [Ca2+]i elicited by 20 mM caffeine, but did not have an effect on the increase induced by 1 μM thapsigargin, in the presence of external Ca2+. These results suggest that the active sites of (1R,9S)-BHS are mainly L-type Ca2+ channels and caffeine-sensitive Ca2+-permeable channels in PC12 cells. |
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AbstractList | (1R,9S)-β-Hydrastine (BHS) decreases the basal intracellular Ca2+ concentration ([Ca2+]i) in PC12 cells.5) This study examined the effects of (1R,9S)-BHS on [Ca2+]i in PC12 cells. (1R,9S)-BHS at 10--100 μM in combination with a high extracellular K+ level (56 mM) inhibited the release of dopamine in a concentration-dependent manner with an IC50 value of 66.5 μM. BHS at 100 μM inhibited the sustained increase in [Ca2+]i induced by a high K+ level (56 mM), and had an inhibitory effect on the 2 μM nifedipine-induced blockage of the K+-stimulated sustained increase in [Ca2+]i. In addition, (1R,9S)-BHS at 100 μM prevented the rapid and sustained increase in [Ca2+]i elicited by 20 mM caffeine, but did not have an effect on the increase induced by 1 μM thapsigargin, in the presence of external Ca2+. These results suggest that the active sites of (1R,9S)-BHS are mainly L-type Ca2+ channels and caffeine-sensitive Ca2+-permeable channels in PC12 cells. |
Author | Yu Yin, Shou Mei Jin, Chun Kuel Yoo, Se Jung Yang, Yoo Mi Kim, Yu Park, Seung-Kook Koo Lee, Myung Joon Lee, Jae |
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