DEVELOPMENTAL NEUROTOXICITY Role of glycogen synthase kinase-3b in ketamine-induced developmental neuroapoptosis in rats

نویسندگان

  • J. R. Liu
  • C. Baek
  • X. H. Han
  • P. Shoureshi
  • S. G. Soriano
چکیده

Editor’s key points † Ketamine increased neuroapoptosis in neonatal rat pups, which correlated with decreased GSK-3b phosphorylation. † This suggests involvement of this cell survival signalling pathway in anaesthetic neurotoxicity. † Co-administration of lithium mitigated ketamine-induced neurotoxicity and reduction in GSK-3b phosphorylation, providing a potential approach to neuroprotection. Background. Ketamine-induced neuroapoptosis has been attributed to diverse stressrelated mechanisms. Glycogen synthase kinase-3b (GSK-3b) is a multifunctional kinase that is active in neuronal development and linked to neurodegenerative disorders. We hypothesized that ketamine would enhance GSK-3b-induced neuroapopotosis, and that lithium, an inhibitor of GSK-3b, would attenuate this response in vivo.

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تاریخ انتشار 2013