J. Lipid Res.
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A more recent version of this article appeared on January 1, 2008

Papers In Press, published online ahead of print October 23, 2007
J. Lipid Res., doi:10.1194/jlr.M700406-JLR200
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Submitted on September 7, 2007
Revised on October 17, 2007
Accepted on October 23, 2007

Chronic N-methyl-D-aspartate administration increases the turnover of arachidonic acid within brain phospholipids of the unanesthetized rat

Ho-Joo Lee, Jagadeesh S. Rao, Lisa Chang, Stanley I. Rapoport, and Richard P. Bazinet

Nutritional Sciences, University of Toronto, Toronto, ON M5S 3E2

Corresponding Author: richard.bazinet{at}utoronto.ca

Whereas antibipolar drug administration to rats reduces brain arachidonic acid turnover, excessive N-methyl-D-aspartate (NMDA) signaling is thought to contribute to bipolar disorder symptoms and may increase arachidonic acid turnover in rat brain phospholipids. To see if chronic NMDA would increase brain arachidonic acid turnover, rats were daily administered NMDA (25 mg/kg, i.p.) or vehicle for 21 days. In a unanesthetized rat, on day 21, [1-14C]arachidonic acid was infused intravenously and arterial blood plasma was sampled until the animal was killed at 5 min and its microwaved brain was subjected to chemical and radiotracer analysis. Using equations from our in vivo fatty acid model, we found that compared to controls, chronic NMDA increased the net rate of incorporation of plasma unesterified arachidonic acid into brain phospholipids (21-31%) as well as the turnover of arachidonic acid within brain phospholipids (26-37%). These changes were absent 3 hours after a single NDMA injection. The changes, opposite to chronic administration of antimanic drugs to rats, suggest that excessive NMDA signaling via arachidonic acid may be a contributing factor to the manic phase of bipolar disorder and that that chronic NMDA-treated animals may be a model of upregulated arachidonic acid turnover in bipolar disorder.


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