NDLI: Role of protein kinase C in Ca2+ homeostasis disorders in cultured rat neurons during hyperstimulation of glutamate receptors

Content Provider	Springer Nature Link
Author	Persiyantseva, N. A. Birikh, K. R. Dvoretskova, E. A. Pinelis, V. G. Khodorov, B. I.
Copyright Year	2008
Abstract	The primary culture of rat cerebellar neurons was used to study protein kinase C activity, intracellular variations in calcium concentration ([Ca2+]i), changes in the mitochondrial potential, and neuronal death during hyperstimulation of glutamate receptors and after 24-h incubation with phorbol ester. Prolonged exposure of neurons to glutamate (100 µM, 45 min) was followed by the development of delayed calcium dysregulation. Protein kinase C activity depended on the time of cell incubation with glutamate. Protein kinase C activity increased in response to application of glutamate for 15 min. However, protein kinase C activity decreased after 45-min exposure to glutamate and development of delayed calcium dysregulation. Protein kinase C activity was nearly undetected after 24-h preincubation of neurons with phorbol ester. Under these conditions, delayed calcium dysregulation developed more slowly and was observed in a smaller number of neurons. Neuronal death decreased to 2±1%. Our results suggest that protein kinase C plays an important role in death of neurons, which exhibit delayed calcium dysregulation during glutamate treatment.
Starting Page	595
Ending Page	599
Page Count	5
File Format	PDF
ISSN	00074888
Journal	Bulletin of Experimental Biology and Medicine
Volume Number	145
Issue Number	5
e-ISSN	15738221
Language	English
Publisher	Springer US
Publisher Date	2008-10-08
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	protein kinase C calcium glutamate neurons phorbol ester Laboratory Medicine Pathology Cell Biology Internal Medicine Biomedicine general
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry, Genetics and Molecular Biology

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