Abstract
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 αCaM kinase II was unchanged, whereas Thr286 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.
Original language | English |
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Pages (from-to) | 2393-2396 |
Number of pages | 4 |
Journal | NeuroReport |
Volume | 15 |
Issue number | 15 |
DOIs | |
Publication status | Published - Oct 25 2004 |
Keywords
- Antidepressant
- CaM kinase II
- Hippocampus
- Neuroplasticity
- Phosphorylation
ASJC Scopus subject areas
- Neuroscience(all)