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Mechanism of action of mood stabilizers
Evidence has accumulated that mood stabilizers may act via a modulation of the function of signal transduction mechanisms that transform, via guanine-nucleotide binding (G-) proteins, signals from the outside into intracellular signals such as cyclic AMP or inositol phosphates. Regulators of G- protein signaling (RGS) serve as GTPase-activating proteins for G-proteins of the Gi and Gq classes and negatively regulate signaling via receptors coupled to these G-proteins. Gαs-protein is increased in post-mortem brain and in neutrophils of bipolar patients but not in unipolar patients. Expression of RGS3 and of Gi mRNA is increased in neutrophils of lithium treated patients as compared to untreated patients and controls. The cellular supply of inositol is determined by the activity of the high affinity myo-inositol transporter (SMIT). SMIT is inhibited by chronic treatment with all three known mood stabilizers (lithium, valproate, carbamazepine) and may therefore represent a common target in their mechanism of action. One final common pathway in the mechanism of action of mood stabilizers may be alteration in transcription of genes that are involved in the regulation of cellular resilience and neuroplasticity.