Ketamine-induced neurotoxicity blocked by N-Methyl-D-aspartate is mediated through activation of PKC/ERK pathway in developing hippocampal neurons. Jiang, S., Li, X., Jin, W., Duan, X., Bo, L., Wu, J., Zhang, R., Wang, Y., Kang, R., & Huang, L. Neuroscience Letters, 673:122-131, Elsevier, 3, 2018.
Ketamine-induced neurotoxicity blocked by N-Methyl-D-aspartate is mediated through activation of PKC/ERK pathway in developing hippocampal neurons [link]Website  abstract   bibtex   
Ketamine, a non-competitive N-methyl D-aspartate (NMDA) receptor antagonist, is widely used in pediatric clinical practice. However, prolonged exposure to ketamine results in widespread anesthetic neurotoxicity and long-term neurocognitive deficits. The molecular mechanisms that underlie this important event are poorly understood. We investigated effects of anesthetic ketamine on neuroapoptosis and further explored role of NMDA receptors in ketamine-induced neurotoxicity. Here we demonstrate that ketamine induces activation of cell cycle entry, resulting in cycle–related neuronal apoptosis. On the other hand, ketamine administration alters early and late apoptosis of cultured hippocampus neurons by inhibiting PKC/ERK pathway, whereas excitatory NMDA receptor activation reverses these effects. Ketamine-induced neurotoxicity blocked by NMDA is mediated through activation of PKC/ERK pathway in developing hippocampal neurons.
@article{
 title = {Ketamine-induced neurotoxicity blocked by N-Methyl-D-aspartate is mediated through activation of PKC/ERK pathway in developing hippocampal neurons},
 type = {article},
 year = {2018},
 identifiers = {[object Object]},
 keywords = {Cell cycle re-entry,Hippocampus,Ketamine,NMDA,PKC/ERK signaling pathway},
 pages = {122-131},
 volume = {673},
 websites = {https://www.sciencedirect.com/science/article/abs/pii/S0304394018301332},
 month = {3},
 publisher = {Elsevier},
 day = {1},
 id = {737f73c2-57f5-35e4-ae40-d4938c41ca3e},
 created = {2018-03-09T11:27:00.650Z},
 accessed = {2018-03-09},
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 last_modified = {2018-05-31T16:53:50.187Z},
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 abstract = {Ketamine, a non-competitive N-methyl D-aspartate (NMDA) receptor antagonist, is widely used in pediatric clinical practice. However, prolonged exposure to ketamine results in widespread anesthetic neurotoxicity and long-term neurocognitive deficits. The molecular mechanisms that underlie this important event are poorly understood. We investigated effects of anesthetic ketamine on neuroapoptosis and further explored role of NMDA receptors in ketamine-induced neurotoxicity. Here we demonstrate that ketamine induces activation of cell cycle entry, resulting in cycle–related neuronal apoptosis. On the other hand, ketamine administration alters early and late apoptosis of cultured hippocampus neurons by inhibiting PKC/ERK pathway, whereas excitatory NMDA receptor activation reverses these effects. Ketamine-induced neurotoxicity blocked by NMDA is mediated through activation of PKC/ERK pathway in developing hippocampal neurons.},
 bibtype = {article},
 author = {Jiang, Sufang and Li, Xuze and Jin, Wei and Duan, Xiaofeng and Bo, Lijun and Wu, Jiangli and Zhang, Rui and Wang, Ying and Kang, Rongtian and Huang, Lining},
 journal = {Neuroscience Letters}
}

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