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SMIT1 haploinsufficiency causes brain inositol deficiency without affecting lithium-sensitive behavior
Alona Shaldubina1, Roy A Johanson, W Timothy O'Brien
1Stanley Research Center, Faculty of Health Sciences, Ben Gurion University of the Negev and Mental Health Center, Beer Sheva, Israel.
Molecular Genetics and Metabolism
|April 29, 2006
Summary
Lithium
Area of Science:
- Neuroscience
- Pharmacology
- Genetics
Background:
- Lithium is a mood stabilizer for bipolar disorder.
- Two hypotheses explain lithium's action: inositol depletion and GSK-3 inhibition.
- The role of inositol depletion in lithium's behavioral effects remains untested.
Purpose of the Study:
- To investigate the contribution of inositol depletion to lithium-sensitive behaviors.
- To test the inositol depletion hypothesis of lithium's mechanism of action.
Main Methods:
- Disruption of the sodium myo-inositol transporter 1 (SMIT1) gene in mice.
- Assessment of lithium-sensitive behaviors in SMIT1+/- mice with depleted brain myo-inositol.
- Comparison with previous studies on SMIT-/- mice.
Main Results:
- Depletion of brain myo-inositol in SMIT1+/- mice did not affect lithium-sensitive behavior.
- Previous findings showed greater inositol depletion in SMIT-/- mice without affecting phosphatidylinositol levels.
Conclusions:
- The results challenge the current inositol depletion hypothesis for lithium's action in bipolar disorder.
- The findings suggest that inositol depletion is not the primary mechanism behind lithium-sensitive behaviors.
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