Lithium induced neural plasticity

Neural plasticity refers to the brain’s ability to make new cellular connections. Drugs that can induce neural plasticity are of basic as well as clinical interest. Lithium, a drug already in use, has been demonstrated to be neuroprotective and is likely to find wider use. The spectrum of diseases that can be potentially treated with lithium suggests that there could be a common cellular mechanism, such as neural plasticity, in operation. We review effects of lithium on major cellular processes that comprise neuroplasticity – alterations, in vitro and in vivo, in neurites, axons and synapse formation. Lithium is known to support extension of cytoplasmic outgrowths. Lithium alters patterns of axonal modifications including their extensions or retractions and sprouting of new branches. However, there are few studies directly demonstrating lithium action of synapse formation. The molecular basis of lithium action is complex with various pathways involved in cross talk. Of these multiple pathways, we have focused on lithium induced inhibition of glycogen synthase kinase-3β, block of inositol phosphate pathway and up regulation of neurotrophins as there are direct evidences of involvement of these in lithium induced neuroplasticity. This review provides a bird’s eye view of studies that could provide insight into special aspect of lithium action, induction of plasticity, which have implication for treating a wide variety of neurological conditions