Ketamine-induced neurotoxicity blocked by N -Methyl- d -aspartate is mediated through activation of PKC/ERK pathway in developing hippocampal neurons
| Autor: | Rongtian Kang, Sufang Jiang, Wei Jin, Xuze Li, Rui Zhang, Lining Huang, Lijun Bo, Wu Jiangli, Ying Wang, Xiaofeng Duan |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway N-Methylaspartate MAP Kinase Signaling System medicine.drug_class Hippocampus Apoptosis Hippocampal formation Pharmacology Receptors N-Methyl-D-Aspartate Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine medicine Animals Ketamine Cells Cultured Protein Kinase C Protein kinase C Neurons Anesthetics Dissociative Dose-Response Relationship Drug Chemistry General Neuroscience Cell Cycle Neurotoxicity medicine.disease Receptor antagonist 030104 developmental biology nervous system NMDA receptor 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Neuroscience Letters. 673:122-131 |
| ISSN: | 0304-3940 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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