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Accession number;02A0472875
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| Title;Effects of lithium and valproate on calcium homeostasis. Relevant to the pathophysiology of bipolar disorder. |
| Author;
KUSUMI ICHIRO
(Hokudai Daigakuin'igakukenkyuka Seishin'igaku)
AKIMOTO TATSUYUKI
(Hokudai Daigakuin'igakukenkyuka Seishin'igaku)
SASAKI YUKI
(Hokudai Daigakuin'igakukenkyuka Seishin'igaku)
SUZUKI KATSUJI
(Hokudai Daigakuin'igakukenkyuka Seishin'igaku)
KAMEDA KENSUKE
(Hokudai Daigakuin'igakukenkyuka Seishin'igaku)
KOYAMA TSUKASA
(Hokudai Daigakuin'igakukenkyuka Seishin'igaku)
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Journal Title;Annual Report of the Pharmacopsychiatry Research Foundation
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Journal Code:Y0939A
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ISSN:0286-7591
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VOL.;NO.34;PAGE.65-71(2002)
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| Figure&Table&Reference;FIG.5, TBL.2, REF.15 |
| Pub. Country;Japan |
| Language;Japanese |
| Abstract;We have indicated that agonist-stimulated intraplatelet calcium(Ca) mobilization is enhanced in bipolar disorders. In this study, the effects of lithium and valproate on the agonist-stimulated Ca response were examined in the presence or absence of modulators of two main signal transduction systems, protein kinase C(PKC) and calmodulin(CaM). Pre-incubation with lithium reduced the enhanced Ca response to serotonin(5-HT) induced by CaM antagonist, while it failed to affect the Ca response in the presence of PKC activator or inhibitor. On the other hand, pre-incubation with valproate reversed dose-dependently the inhibition of Ca response induced by PKC activator. Valproate itself significantly inhibited the agonist-stimulated Ca response, which was reversed by addition of PKC inhibitor. These findings suggest that the mechanism of action of lithium and valproate may be mainly involved in the CaM and PKC pathways, respectively. (author abst.) |
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