Calcium-dependent protein kinase C activation in acutely isolated neurons during oxygen and glucose deprivation

Glutamate excitotoxicity and necrotic cell death are characteristic features of ischemic neuronal injury. In the penumbral area, glutamate exposure is less pronounced and neuronal death is delayed. Recent studies suggest that delayed neuronal death is propagated by intracellular signalling pathways....

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Bibliographic Details
Published in:Neurochemical research 2004-10, Vol.29 (10), p.1931-1937
Main Authors: Larsen, Geir Arne, Berg-Johnsen, Jon, Moe, Morten C, Vinje, Morten Larsen
Format: Article
Language:English
Subjects:
Animals
Cell Hypoxia - physiology
Cell Separation - methods
Enzyme Activation - physiology
Female
Glucose - metabolism
Neurons - enzymology
Oxygen - metabolism
Protein Kinase C - metabolism
Rats
Rats, Wistar
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Summary:Glutamate excitotoxicity and necrotic cell death are characteristic features of ischemic neuronal injury. In the penumbral area, glutamate exposure is less pronounced and neuronal death is delayed. Recent studies suggest that delayed neuronal death is propagated by intracellular signalling pathways. Protein kinase C (PKC) activation may initiate apoptosis, but its role in ischemia is still not clear. In this study the PKC activity was investigated during non-excitotoxic ischemia in acutely dissociated rat CA1 neurons. During oxygen and glucose deprivation (OGD) the PKC activity measured with the fluorescent dye Fim-1 increased rapidly reaching a maximum of 31+/-8% (P < 0.05) after 5 min. When extracellular Ca2+ was depleted, the fluorescence intensity increased by 20+/-8% (P
ISSN:0364-3190
1573-6903
DOI:10.1023/B:NERE.0000042220.16373.29