• Int. J. Dev. Neurosci. · Jun 2011

    MEK/ERKs signaling is essential for lithium-induced neurite outgrowth in N2a cells.

    • Zhuyao Wang, Juan Wang, Jingjin Li, Xiaohui Wang, Yuzhen Yao, Xiaojin Zhang, Chuanfu Li, Yunlin Cheng, Guoxian Ding, Li Liu, and Zhengnian Ding.
    • Department of Geriatrics, First Affiliated Hospital with Nanjing Medical University, Guangzhou Road 300, Nanjing 210029, China.
    • Int. J. Dev. Neurosci. 2011 Jun 1;29(4):415-22.

    AbstractLithium, a drug used for the treatment of bipolar disorder, has been shown to affect different aspects of neuronal development such as neuritogenesis, neurogenesis and survival. The underlying mechanism responsible for lithium's influence on neuronal development, however, still remains to be elucidated. In the present study, we demonstrate that lithium increases the phosphorylation of extracellular-signal regulated kinases (ERKs) and protein kinase B (Akt) and promotes neurite outgrowth in mouse N2a neuroblastoma cells (N2a). The inactivation of mitogen-activated protein kinase kinase (MEK)/ERKs signaling with a MEK inhibitor inhibits neurite outgrowth, but it enhances Akt activation in lithium-treated N2a cells. Furthermore, the inactivation of phosphoinositide-3-kinase (PI3K)/Akt signaling with a PI3K inhibitor increases both lithium-induced ERKs activation and lithium-induced neurite outgrowth. Taken together, our study suggests that lithium-induced neurite outgrowth in N2a cells is regulated by cross-talk between the MEK/ERKs and PI3K/Akt pathways and requires the activation of the MEK/ERKs signaling.Copyright © 2011 ISDN. Published by Elsevier Ltd. All rights reserved.

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