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 aCaM 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 cultureswith reboxetine reduced kinase activation in a concentration-dependentmanner.The short-terminhibitory e¡ect of reboxetine suggests that kinase up-regulation during antidepressant drug treatment is an adaptive response compensating for initial functional down-regulation.

Antidepressants activate CaMKII in neuron cell body by Thr286 phosphorylation / E. Tiraboschi, R. Giambelli, G. D'Urso, A. Galietta, A. Barbon, A. de Bartolomeis, M. Gennarelli, S. Barlati, G. Racagni, M. Popoli. - In: NEUROREPORT. - ISSN 0959-4965. - 15:15(2004), pp. 2393-2396.

Antidepressants activate CaMKII in neuron cell body by Thr286 phosphorylation

E. Tiraboschi
Primo
;
G. Racagni
Penultimo
;
M. Popoli
Ultimo
2004

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 aCaM 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 cultureswith reboxetine reduced kinase activation in a concentration-dependentmanner.The short-terminhibitory e¡ect of reboxetine suggests that kinase up-regulation during antidepressant drug treatment is an adaptive response compensating for initial functional down-regulation.
Antidepressant ; CaMkinase II ; Hippocampus ; Neuroplasticity ; Phosphorylation
Settore BIO/14 - Farmacologia
2004
http://journals.lww.com/neuroreport/pages/default.aspx
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/145362
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