scholarly journals Protective Effect of (4-Methoxybenzylidene)-(3-methoxynophenyl)amine against Neuronal Cell Death Induced by Oxygen and Glucose Deprivation in Rat Organotypic Hippocampal Slice Culture

2007 ◽  
Vol 30 (1) ◽  
pp. 189-192 ◽  
Author(s):  
Sang Yoon Choi ◽  
Sanghee Kim ◽  
Dongwook Son ◽  
Pyeongjae Lee ◽  
Jongseok Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Protective Effect ◽  
Hippocampal Slice ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Glucose Deprivation ◽  
Slice Culture ◽  
Oxygen And Glucose Deprivation ◽  
Organotypic Hippocampal Slice Culture ◽  
Hippocampal Slice Culture

scholarly journals Characterization of the Postconditioning Effect of Dexmedetomidine in Mouse Organotypic Hippocampal Slice Cultures Exposed to Oxygen and Glucose Deprivation

2010 ◽  
Vol 112 (2) ◽  
pp. 373-383 ◽  
Author(s):  
Souhayl Dahmani ◽  
Danielle Rouelle ◽  
Pierre Gressens ◽  
Jean Mantz
Keyword(s):  
Cell Death ◽  
Focal Adhesion ◽  
Hippocampal Slice ◽  
Glucose Deprivation ◽  
Slice Culture ◽  
Oxygen And Glucose Deprivation ◽  
Organotypic Hippocampal Slice Culture ◽  
Hippocampal Slice Culture ◽  
Maximum Cell ◽  
Pharmacologic Modulation

Background There is an increasing interest in the use of dexmedetomidine for anesthesia and sedation. Here, we used the mouse organotypic hippocampal slice culture to investigate whether dexmedetomidine exhibits postconditioning properties against oxygen and glucose deprivation (OGD). The role of the focal adhesion and extracellular-regulated kinases pathways in these effects were examined in both postconditioning and preconditioning. Materials and Methods Slices were obtained from P5 mouse. In postconditioning experiments, Dexmedetomidine (1 microm) was incubated 60 min after the end of OGD. In preconditioning experiments, dexmedetomidine was applied 3 h before OGD. Pharmacologic modulation of the studied pathways was achieved by using selective inhibitors of these cascades. Cell death was assessed 72 h after OGD using propidium iodide labeling and protein expression of activated caspase 3. Results Maximum cell death increased with the duration of OGD. Dexmedetomidine induced a postconditioning effect in the CA1 (but not dentate gyrus) subfield area, which was significantly reduced by modulators of the focal adhesion and the extracellular-regulated kinases pathways. The combination of the inhibitors of the two pathways completely abolished the postconditioning effect of dexmedetomidine. The preconditioning effect of dexmedetomidine against ischemia-induced injury was observed in all hippocampal subfield areas. Results obtained with the pharmacologic modulation used for postconditioning also applied to dexmedetomidine-induced preconditioning. Discussion Dexmedetomidine exhibits significant, but moderate, postconditioning properties against oxygen and glucose deprivation-induced injury. Activation of focal adhesion and the imidazoline 1 receptors-extracellular-regulated kinases pathways is involved in dexmedetomidine-induced postconditioning and preconditioning as well.

scholarly journals Epsilon Protein Kinase C Mediated Ischemic Tolerance Requires Activation of the Extracellular Regulated Kinase Pathway in the Organotypic Hippocampal Slice

2004 ◽  
Vol 24 (6) ◽  
pp. 636-645 ◽  
Author(s):  
Christian Lange-Asschenfeldt ◽  
Ami P. Raval ◽  
Kunjan R. Dave ◽  
Daria Mochly-Rosen ◽  
Thomas J. Sick ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Hippocampal Slice ◽  
Glucose Deprivation ◽  
Mitogen Activated Protein Kinase ◽  
Slice Culture ◽  
Erk Pathway ◽  
Organotypic Hippocampal Slice Culture ◽  
Hippocampal Slice Culture ◽  
Kinase C

Ischemic preconditioning (IPC) promotes brain tolerance against subsequent ischemic insults. Using the organotypic hippocampal slice culture, we conducted the present study to investigate (1) the role of adenosine A1 receptor (A1AR) activation in IPC induction, (2) whether epsilon protein kinase C (ɛPKC) activation after IPC is mediated by the phosphoinositol pathway, and (3) whether ɛPKC protection is mediated by the extracellular signal-regulated kinase (ERK) pathway. Our results demonstrate that activation of A1AR emulated IPC, whereas blockade of the A1AR during IPC diminished neuroprotection. The neuroprotection promoted by the A1AR was also reduced by the ɛPKC antagonist. To determine whether ɛPKC activation in IPC and A1AR preconditioning is mediated by activation of the phosphoinositol pathway, we incubated slices undergoing IPC or adenosine treatment with a phosphoinositol phospholipase C inhibitor. In both cases, preconditioning neuroprotection was significantly attenuated. To further characterize the subsequent signal transduction pathway that ensues after ɛPKC activation, mitogen-activated protein kinase kinase was blocked during IPC and pharmacologic preconditioning (PPC) (with ɛPKC, NMDA, or A1AR agonists). This treatment significantly attenuated IPC- and PPC-induced neuroprotection. In conclusion, we demonstrate that ɛPKC activation after IPC/PPC is essential for neuroprotection against oxygen/glucose deprivation in organotypic slice cultures and that the ERK pathway is downstream to ɛPKC.

scholarly journals Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death

Redox Report ◽  
2021 ◽  
Vol 26 (1) ◽  
pp. 53-61
Author(s):  
Mi Hye Kim ◽  
Da Yeon Kim ◽  
Hong Jun Lee ◽  
Young-Ho Park ◽  
Jae-Won Huh ◽  
...  
Keyword(s):  
Cell Death ◽  
Protective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell
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