The high affinity inositol transport system--implications for the pathophysiology and treatment of bipolar disorder.
Bipolar Disord
; 2(2): 102-7, 2000 Jun.
Article
en En
| MEDLINE
| ID: mdl-11252649
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.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Trastorno Bipolar
/
Proteínas Portadoras
/
Compuestos de Litio
/
Antimaníacos
/
Simportadores
/
Proteínas de Choque Térmico
/
Inositol
/
Proteínas de la Membrana
Límite:
Humans
Idioma:
En
Revista:
Bipolar Disord
Asunto de la revista:
PSIQUIATRIA
Año:
2000
Tipo del documento:
Article
País de afiliación:
Alemania
Pais de publicación:
Dinamarca