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(1) We favour a hypothesis that the delayed <neuronal injury> in <hippocampus> is iniated by the increase of intracellular <calcium> concentration, activating transiently Ca-dependent <protein kinase>.(2) The secondary effects of the <postischemic>, short-lasting PKC translocation/activation could involve:an activation of cAMP signaling pathway; an activation of early response <protein> like <ornitine decarboxylase>.
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25-29
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author
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paper
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Barbara Zablocka
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bwmeta1.element.element-from-psjc-af4d8287-f107-3552-b4f0-db8dd51f7989