Abstract:
:Lithium has been proven to be effective in the therapy of bipolar disorder, but its mechanism of pharmacological action is not clearly defined. We examined the effects of lithium on voltage-dependent Na(+) channels, nicotinic acetylcholine receptors, and voltage-dependent Ca(2+) channels, as well as catecholamine secretion in cultured bovine adrenal chromaffin cells. Lithium chloride (LiCl) reduced veratridine-induced (22)Na(+) influx in a concentration-dependent manner, even in the presence of ouabain, an inhibitor of Na(+), K(+)-ATPase. Glycogen synthase kinase-3 (GSK-3) inhibitors (SB216763, SB415286 or the GSK-3 inhibitor IX) did not affect veratridine-induced (22)Na(+) influx, as well as inhibitory effect of LiCl on veratridine-induced (22)Na(+) influx. Enhancement of veratridine (site 2 toxin)-induced (22)Na(+) influx caused by alpha-scorpion venom (site 3 toxin), beta-scorpion venom (site 4 toxin), or Ptychodiscus brevis toxin-3 (site 5 toxin), still occurred in the presence of LiCl in the same manner as in the control cells. LiCl also reduced veratridine-induced (45)Ca(2+) influx and catecholamine secretion. In contrast, LiCl (< or = 30 mM) had no effect on nicotine-induced (22)Na(+) influx, (45)Ca(2+) influx and catecholamine secretion, as well as on high K(+)-induced (45)Ca(2+) influx and catecholamine secretion. Chronic treatment with LiCl at 100mM (but not at < or = 30 mM) significantly reduced cell viability in a time-dependent manner. These results suggest that lithium selectively inhibits Na(+) influx thorough Na(+) channels and subsequent Ca(2+) influx and catecholamine secretion, independent of GSK-3 inhibition.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Yanagita T,Maruta T,Uezono Y,Satoh S,Yoshikawa N,Nemoto T,Kobayashi H,Wada Adoi
10.1016/j.neuropharm.2007.08.018subject
Has Abstractpub_date
2007-12-01 00:00:00pages
881-9issue
7eissn
0028-3908issn
1873-7064pii
S0028-3908(07)00274-2journal_volume
53pub_type
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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doi:10.1016/j.neuropharm.2006.08.009
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journal_title:Neuropharmacology
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doi:10.1016/j.neuropharm.2007.12.005
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
pub_type: 杂志文章
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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doi:10.1016/j.neuropharm.2017.01.009
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journal_title:Neuropharmacology
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pub_type: 杂志文章
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journal_title:Neuropharmacology
pub_type: 杂志文章,评审
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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doi:10.1016/j.neuropharm.2004.12.024
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