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Nicotine‐induced phosphorylation of Akt through epidermal growth factor receptor and Src in PC12h cells

Nicotine treatment triggers calcium influx into neuronal cells, which promotes cell survival in a number of neuronal cells. Phosphoinositide (PI) 3‐kinase and downstream PI3‐kinase target Akt have been reported to be important in the calcium‐mediated promotion of survival in a wide variety of cells. We investigated the mechanisms of nicotine‐induced phosphorylation of Akt in PC12h cells, in comparison with nicotine‐induced ERK phosphorylation. Nicotine induced Akt phosphorylation in a dose‐dependent manner. A nicotinic acetylcholine receptor (nAChR) α7 subunit‐selective inhibitor had no significant effect on nicotine‐induced Akt phosphorylation, while a non‐selective nAChR antagonist inhibited the phosphorylation. L‐type voltage‐sensitive calcium channel (VSCC) antagonists, calmodulin antagonist, and Ca2+/calmudulin‐dependent protein kinase (CaM kinase) inhibitor prevented the nicotine‐induced Akt phosphorylation. Three epidermal growth factor receptor (EGFR) inhibitors prevented the nicotine‐induced phosphorylation of both extracellular signal‐regulated protein kinase (p42/44 MAP kinase, ERK) and Akt. In contrast, an inhibitor of the Src family tyrosine kinase prevented the nicotine‐induced Akt phosphorylation but not ERK phosphorylation. These results suggested that nicotine induces the activation of both PI3‐kinase/Akt and ERK pathways via common pathways including non‐α7‐nAChRs, L‐type VSCC, CaM kinase II and EGFR in PC12h cells, but Src family tyrosine kinases only participate in the pathway to activate Akt.