Recently, special attention has been given to the possible neuroprotective effects of lithium, especially by the discovery of its regulatory effects on pro and anti-apoptotic proteins. Lithium substantially increases the cytoprotective proteins expression in the central nervous system, both in rat cortex and in human cells of neuronal origin. In addition to neuroprotective actions, it aids in the regeneration of axons in the central nervous system of mammals. Lithium negatively regulates the expression and activity of enzymes that exert important functions in cerebral homeostasis, regulating glycogen synthesis under the influence of the insulin cascade beside the cytoskeleton remodeling (synaptic plasticity, neurogenesis, and phosphorylation of tau protein). Microglia is known for its importance in neuropathologies. However, under physiological conditions, such immune cells interact actively with neurons, being able to modulate the fate and functions of the synapses. Such ability of microglial cells suggests the consequences of changes in microglial phenotype under pathological conditions, which makes it relevant to understand the interaction between microglial and other developing brain cells and their influence on the formation of neuronal and synaptic networks. The current work aims to identify the main pathway of neuronal-glia integration activated by chronic treatment with lithium in neurons, exploring the use of bioinformatics tools in microarray data.
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