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An animal model for mania: preliminary results
R S el-Mallakh1, L T Harrison, R Li
1Mood Disorders Research Program, University of Louisville School of Medicine, Kentucky, USA.
Progress in Neuro-Psychopharmacology & Biological Psychiatry
|September 1, 1995
Summary
Decreased sodium-potassium adenosine triphosphatase (Na,K-ATPase) activity is linked to bipolar disorder. This study used ouabain in rats to model mania, suggesting a potential role for Na,K-ATPase inhibition in the illness.
Area of Science:
- Neuroscience
- Biochemistry
- Psychiatry
Background:
- Human bipolar patients exhibit reduced membrane Na,K-ATPase activity during both manic and depressive episodes.
- Digoxin neurotoxicity, known to affect Na,K-ATPase, can induce mania or depression symptoms.
Purpose of the Study:
- To investigate the hypothesis that central nervous system Na,K-ATPase inhibition contributes to the pathophysiology of bipolar illness.
- To establish a potential animal model for mania based on biochemical alterations observed in humans.
Main Methods:
- Rats were administered ouabain, a cardiac glycoside that inhibits Na,K-ATPase, via intracerebroventricular (i.c.v.) injection at sublethal doses.
- Behavioral activity was quantified by measuring total square crossings in an open-field test.
Main Results:
- Intracerebroventricular administration of 5 microliters of 10(-3) M ouabain significantly increased motor activity in rats.
- This increase in motor activity suggests a potential animal model for manic states.
Conclusions:
- Central nervous system Na,K-ATPase inhibition may play a role in the development of bipolar disorder.
- Intracerebroventricular ouabain administration in rats presents a promising preliminary animal model for mania, correlating with human biochemical findings.