Role of protein kinase C in Ca(2+) homeostasis disorders in cultured rat neurons during hyperstimulation of glutamate receptors.

Abstract:

:The primary culture of rat cerebellar neurons was used to study protein kinase C activity, intracellular variations in calcium concentration ([Ca(2+)]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 microM, 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.

journal_name

Bull Exp Biol Med

authors

Persiyantseva NA,Birikh KR,Dvoretskova EA,Pinelis VG,Khodorov BI

doi

10.1007/s10517-008-0159-6

subject

Has Abstract

pub_date

2008-05-01 00:00:00

pages

595-9

issue

5

eissn

0007-4888

issn

1573-8221

pii

doi

journal_volume

145

pub_type

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