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A complex intercellular and intracellular signaling network modulates the main neural functions. Regulation of protein kinases and protein phosphatases activities modify the phosphorylation state of target proteins that direct a diversity of cell fates, including gene expression, neural cell migration, differentiation or proliferation, cell survival or death, and synaptic plasticity. Regardless of all these aspects, modulation of intracellular signaling pathways by toxicants has only recently become part of the molecular toxicology research. Manganese (Mn) exposure causes a neurological syndrome, manganism, which resembles Parkinson's disease. The mechanisms of Mn neurotoxicity are not completely clear but may involve mitochondrial dysfunctions, induction of oxidative stress, and alterations in dopaminergic system, especially in the basal ganglia. The modulation of intracellular cell signaling elements by Mn and the cell fates of these effects is an issue that requires attention. In this chapter, we will present cell signaling pathways dependent of protein kinases (e.g. PKA, PKC, MAPKs, AKT, and GSK3β) and protein phosphatases (e.g. PP1 and PP2A) that have been reported to be altered in response to Mn exposure. Since only a few studies have addressed these aspects in vivo, a series of data obtained in vitro from cell cultures exposed to Mn will also be presented, aiming to help us identify the possible sites of Mn action in cell signaling networks involved in the patophysiology of Mn neurotoxicity.

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