DEVELOPMENTAL NEUROTOXICITY Role of glycogen synthase kinase-3b in ketamine-induced developmental neuroapoptosis in rats
نویسندگان
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.
منابع مشابه
Glycogen synthase kinase-3β may contribute to neuroprotective effects of Sargassum oligocystum against amyloid-beta in neuronal SH-SY5Y cells
Glycogen synthase kinase (GSK)-3β mediates amyloid-beta (Aβ) and oxidative stress-induced neurotoxicity in neurodegenerative disorders. Natural products with antioxidant activity, such as Sargassum (S.) oligocystum may modulate GSK-3β enzyme and protect against Aβ-induced neurotoxicity. Therefore, we aimed to assess the neuroprotective effects of a methanolic extract of S. oligocystum against A...
متن کاملThe neuroprotective mechanism of cinnamaldehyde against amyloid-β in neuronal SHSY5Y cell line: The role of N-methyl-D-aspartate, ryanodine, and adenosine receptors and glycogen synthase kinase-3β
Objective: Cinnamaldehyde may be responsible for some health benefits of cinnamon such as its neuroprotective effects. We aimed to investigate the cinnamaldehyde neuroprotective effects against amyloid beta (Aβ) in neuronal SHSY5Y cells and evaluate the contribution of N-methyl-D-aspartate (NMDA), ryanodine, and adenosine receptors and glycogen ...
متن کاملLithium protects against anesthesia-induced developmental neuroapoptosis.
BACKGROUND Ethanol and anesthetic drugs trigger neuroapoptosis in the developing mouse brain. Recently, it was found that ethanol-induced neuroapoptosis is preceded by suppressed phosphorylation of extracellular signal-regulated protein kinase (ERK), and lithium counteracts both the phosphorylated ERK suppressant action and ethanol-induced neuroapoptosis. The current study was undertaken to add...
متن کاملThe Potential Role of Glycogen Synthase Kinase-3β in Neuropathy-Induced Apoptosis in Spinal Cord
Introduction: Glycogen Synthase Kinase-3β (GSK-3β) participates in several signaling pathways and plays a crucial role in neurodegenerative diseases, inflammation, and neuropathic pain. The ratio of phosphorylated GSK-3β over total GSK-3β (p-GSK-3β/t-GSK-3β) is reduced following nerve injury. Apoptosis is a hallmark of many neuronal dysfunctions in the context of neuropathic pain. Thus, this st...
متن کاملLithium-Mediated Protection Against Ethanol Neurotoxicity
Lithium has long been used as a mood stabilizer in the treatment of manic-depressive (bipolar) disorder. Recent studies suggest that lithium has neuroprotective properties and may be useful in the treatment of acute brain injuries such as ischemia and chronic neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis. One ...
متن کامل