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Kirshenbaum, Greer S; Clapcote, Steven J; Duffy, Steven; Burgess, Christian R; Petersen, Janne; Jarowek, Karolina J; Yücel, Yeni H; Cortez, Miguel A; Snead, O. Carter III; Vilsen, Bente; Peever, John H; Ralph, Martin R; Roder, John C
Proceedings of the National Academy of Sciences - PNAS, 11/2011, Volume: 108, Issue: 44Journal Article
Bipolar disorder is a debilitating psychopathology with unknown etiology. Accumulating evidence suggests the possible involvement of Na+,K+-ATPase dysfunction in the pathophysiology of bipolar disorder. Here we show that Myshkin mice carrying an inactivating mutation in the neuron-specific Na+,K+-ATPase α3 subunit display a behavioral profile remarkably similar to bipolar patients in the manic state. Myshkin mice show increased Ca2+ signaling in cultured cortical neurons and phospho-activation of extracellular signal regulated kinase (ERK) and Akt in the hippocampus. The mood-stabilizing drugs lithium and valproic acid, specific ERK inhibitor SL327, rostafuroxin, and transgenic expression of a functional Na+,K+-ATPase α3 protein rescue the mania-like phenotype of Myshkin mice. These findings establish Myshkin mice as a unique model of mania, reveal an important role for Na+,K+-ATPase α3 in the control of mania-like behavior, and identify Na+,K+-ATPase α3, its physiological regulators and downstream signal transduction pathways as putative targets for the design of new antimanic therapies.
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