Abstract
Lithium salt has been widely used as a treatment for mania, but the mechanism of its effect remains unknown. Previously, by studying c-fos expression, we showed that the striatum was a possible target region for the antimanic effects of lithium salt. The present study focused on the effect of subchronic lithium chloride treatment on G-proteins (G olf, Gγ 7) and adenylyl cyclase type V, which are expressed specifically in the rat striatum. Subchronic lithium chloride treatment significantly increased the level of G olf protein, a stimulant α-subunit of G-protein, by 53.5% ( P<0.01), but the levels of Gγ 7 and adenylyl cyclase type V did not change. This increased level of G olf protein was found after 2 weeks of lithium chloride treatment, but not after 1 week, and the level returned to the basal level 1 week after withdrawal of lithium chloride. This result suggests that the level of G olf protein increases to compensate for the suppression of the adenylyl cyclase system by lithium, and that this increase may account for the “rebound” phenomenon, which is the relapse observed after abrupt discontinuation of lithium salt treatment.
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