Methylphenidate alters Akt‐mTOR signaling in rat pheochromocytoma cells

摘要: Abstract The exponential increase in methylphenidate (MPH) prescriptions recent years has worried researchers about its misuse among individuals who do not meet the full diagnostic criteria for attention-deficit/hyperactivity disorder (ADHD) such as young children and students search of cognitive improvement or recreational reasons. action MPH is based mainly on inhibition dopamine transporter, but complete cellular effects are still unknown. Based upon prior studies, we attempted to determine whether treatment with (1μM) influences protein kinase B-mammalian target rapamycin complex 1 signaling pathways (Akt-mTOR), including translation repressor (4E-BP1) mitogen activated (S6K), rat pheochromocytoma cells (PC12), a well characterized model, long short term. Akt substrates [cAMP response element-binding (CREB), forkhead box O1 (FoxO1), glycogen synthase 3 beta (GSK-3β)] were also evaluated. Whereas term decreased pAkt/Akt, pmTOR/mTOR pS6K/S6K ratios, pFoxO1 immunocontent PC12 cells, increased pGSK-3β/GSK-3β ratio. Phosphorylation levels 4E-BP1 at 15 30 min 6 h by MPH. pCREB/CREB ratio was decreased. This study shows that Akt-mTOR pathway, other important which have been described regulators synthesis, being implicated survival, synaptic plasticity memory consolidation, affected representing an step exploring effects.