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We previously showed that the mood stabilizers lithium, valproate (VPA), and carbamazepine (CBZ) have a common, inositol-reversible effect on the dynamic behavior of sensory neurons, suggesting that they all inhibit phosphoinositide (PIns) synthesis. We now report similar effects of the drugs in cortical neurons and show by mRNA analysis that these neurons do not express myo-inositol-1-phosphate synthase (MIP-synthase) or the sodium-dependent myo-inositol transporters (SMIT1 and SMIT2), but they do express the H+/myo-inositol transporter (HMIT) mRNA and protein. We used glycogen synthase kinase-3 (GSK3) inhibitors and Western blotting of GSK3 targets to confirm that the common effects of the drugs on both sensory and cortical neuron growth cones are inositol-dependent and GSK3-independent. Moreover, the anti-convulsant drugs gabapentin and phenytoin do not mimic the mood stabilizers. These results confirm that the common inositol-reversible effect of mood stabilizers on neurons does not involve GSK3 and further show that the effects are independent of MIP-synthase and SMIT transporters.

Original publication




Journal article


Mol Cell Neurosci

Publication Date





27 - 36


Animals, Animals, Newborn, Antimanic Agents, Carbamazepine, Cells, Cultured, Cerebral Cortex, Enzyme Inhibitors, Ganglia, Spinal, Glucose Transport Proteins, Facilitative, Glycogen Synthase Kinase 3, Growth Cones, Lithium, Myo-Inositol-1-Phosphate Synthase, Neurons, Neurons, Afferent, RNA, Messenger, Rats, Rats, Sprague-Dawley, Signal Transduction, Symporters, Valproic Acid