Antidepressants activate CaMKII in neuron cell body by Thr286 phosphorylation

Ettore Tiraboschi, Roberto Giambelli, Giordano D'Urso, Antonio Galietta, Alessandro Barbon, Andrea De Bartolomeis, Massimo Gennarelli, Sergio Barlati, Giorgio Racagni, Maurizio Popoli

Research output: Contribution to journalArticlepeer-review


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 languageEnglish
Pages (from-to)2393-2396
Number of pages4
Issue number15
Publication statusPublished - Oct 25 2004


  • Antidepressant
  • CaM kinase II
  • Hippocampus
  • Neuroplasticity
  • Phosphorylation

ASJC Scopus subject areas

  • Neuroscience(all)


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