Abstract
Lithium, used to treat bipolar disorder, has been reported to decrease rat brain mRNA and protein levels of cytosolic phospholipase A 2 (cPLA 2), an enzyme that selectively hydrolyzes arachidonic acid from the stereospecifically numbered ( sn)-2 position of membrane phospholipids, and to decrease PLA 2 activity. cPLA 2 can be activated by being phosphorylated at its Ser-228, Ser-505, and Ser-727 sites. In this study, we show that the percent phosphorylated cPLA 2 protein in rat brain is unaffected by lithium. Male Fischer-344 rats were fed lithium chloride for 6 weeks, so as to produce a therapeutically equivalent brain lithium concentration; control rats were fed lithium-free chow under parallel conditions. cPLA 2 was immunoprecipitated from brain homogenate and phosphorylated cPLA 2 protein was quantified using an anti-phosphoserine antibody, and compared to net cPLA 2 protein. The mean ratio of phosphorylated/total cPLA 2 was not changed significantly in the lithium-treated compared to the control group. Thus, decreased brain PLA 2 enzyme activity caused by chronic lithium is likely a consequence only of lithium’s downregulation of cPLA 2 transcription.
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