Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cellular model for bipolar illness is presented. It is propounded that alterations in the activity of the membrane sodium- and potassium-activated adenosine triphosphatase pump (Na,K-ATPase) may be responsible for alterations in neuronal excitability and activity. Specifically, a reduction in Na,K-ATPase activity can lead to both mania and depression by increasing membrane excitability and decreasing neurotransmitter release, respectively. Supporting evidence is reviewed, and clinical and research implications are discussed.
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PMID:The Na,K-ATPase hypothesis for bipolar illness. 771 Nov 60

Both mania and bipolar depression have been associated with decrements in the activity of the sodium and potassium-activated adenosine triphosphatase (Na,K-ATPase) membrane pump. Although the role of this observation in the pathophysiology of bipolar illness is unclear, it has been proposed that this defect could be central to the pathogenesis of the illness. In an effort to test this hypothesis, the authors examined the efficacy of lithium pretreatment in attenuating behavioral changes secondary to acute administration of a single intracerebroventricular (i.c.v.) dose of the Na,K-ATPase-inhibiting compound, ouabain, in the Sprague-Dawley rat. Ouabain (10(-3)M) significantly decreased motor activity in automated activity monitors. Lithium pretreatment for 7 d totally prevented this effect. These preliminary data suggest that i.c.v. ouabain administration in the rat may prove to be a viable animal model for bipolar illness.
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PMID:Lithium prevents ouabain-induced behavioral changes. Toward an animal model for manic depression. 927 Oct 6