Abstract
The 'inositol-depletion hypothesis' postulates that the therapeutic effects of lithium are due to inhibition of inositol monophosphatase, which leads to depletion of brain cells of myo-inositol and consequently to dampening of phosphoinositide (PI) signaling. This article examines the potential relevance of an alternative mechanism for inositol depletion: inhibition of myo-inositol uptake that proceeds via the sodium/myo-inositol cotransport (SMIT). We discuss recent in vitro experiments that show a pronounced downregulation of SMIT after chronic treatment with lithium, carbamazepine, and valproate at therapeutically relevant concentrations. It is concluded that downregulation of SMIT could represent a common mechanism of action of mood stabilizers.
| Original language | English |
|---|---|
| Pages (from-to) | 102-107 |
| Number of pages | 6 |
| Journal | Bipolar Disorders |
| Volume | 2 |
| Issue number | 2 |
| DOIs | |
| State | Published - 1 Jan 2000 |
Keywords
- Inositol depletion
- Mood stabilizers
- Myo-inositol uptake
ASJC Scopus subject areas
- Psychiatry and Mental health
- Biological Psychiatry
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