Journal
NEUROREPORT
Volume 15, Issue 15, Pages 2393-2396Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200410250-00018
Keywords
antidepressant; CaM kinase II; hippocampus; neuroplasticity; phosphorylation
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CaM kinase II, a regulator of synaptic plasticity, is implicated in pathophysiology and pharmacology of psychiatric disorders. Chronic treatment with antidepressants desipramine and reboxetine up-regulated CaM kinase II in neuronal cell bodies of hippocampus. mRNA/protein expression for alphaCaM kinase II was unchanged, whereas Thr(286) phosphorylation was increased in pyramidal/granular cell bodies, suggesting that increased phosphorylation is responsible for kinase activation. Short-term treatment of neuronal cultures with reboxetine reduced kinase activation in a concentration-dependent manner. The short-term inhibitory effect of reboxetine suggests that kinase up-regulation during antidepressant drug treatment is an adaptive response compensating for initial functional down-regulation.
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