The high affinity inositol transport system -implications for the pathophysiology and treatment of bipolar disorder

Dietrich Van Calker, Robert H. Belmaker

    Research output: Contribution to journalShort surveypeer-review

    51 Scopus citations

    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 languageEnglish
    Pages (from-to)102-107
    Number of pages6
    JournalBipolar Disorders
    Volume2
    Issue number2
    DOIs
    StatePublished - 1 Jan 2000

    Keywords

    • Inositol depletion
    • Mood stabilizers
    • Myo-inositol uptake

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