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Titolo:
Modifications in brain CaM kinase II after long-term treatment with desmethylimipramine
Autore:
Consogno, E; Racagni, G; Popoli, M;
Indirizzi:
Univ Milan, Inst Pharmacol Sci, Ctr Neuropharmacol, I-20133 Milan, Italy Univ Milan Milan Italy I-20133 Ctr Neuropharmacol, I-20133 Milan, Italy FBF, IRCCS Ctr S Giovanni di Dio, Brescia, Italy FBF Brescia ItalyFBF, IRCCS Ctr S Giovanni di Dio, Brescia, Italy Univ Naples Federico II, Dept Neurol Sci, Naples, Italy Univ Naples Federico II Naples Italy II, Dept Neurol Sci, Naples, Italy
Titolo Testata:
NEUROPSYCHOPHARMACOLOGY
fascicolo: 1, volume: 24, anno: 2001,
pagine: 21 - 30
SICI:
0893-133X(200101)24:1<21:MIBCKI>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT PROTEIN-KINASE; ANTIDEPRESSANT DRUGS; TRANSMITTER RELEASE; HIPPOCAMPAL SLICES; SEROTONIN REUPTAKE; RAT HIPPOCAMPUS; MUTANT MICE; SYNAPSIN-I; CALMODULIN; AUTOPHOSPHORYLATION;
Keywords:
antidepressant; depression; protein phosphorylation; CaM kinase; synaptic vesicle; synaptic plasticity;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Popoli, M Univ Milan, Inst Pharmacol Sci, Ctr Neuropharmacol, Via Balzaretti 9, I-20133 Milan, Italy Univ Milan Via Balzaretti 9 Milan Italy I-2013333 Milan, Italy
Citazione:
E. Consogno et al., "Modifications in brain CaM kinase II after long-term treatment with desmethylimipramine", NEUROPSYCH, 24(1), 2001, pp. 21-30

Abstract

The present study investigated the effect of long-term (15 mg/kg for 15 days) and acute (15 mg/kg, single administration) treatment with desmethylimipramine, a tricyclic antidepressant drug, on calcium/calmodulin-dependent protein kinase II (CaMKII), a kinase implicated in the mechanism of antidepressant drug action. Similar to selective and non-selective serotonin reuptake inhibitors, long-term, but not acute, treatment with desmethylimipraminemarkedly increased the activity of CaMKII in the hippocampal synaptic vesicle fraction (+51.9%). The kinase activity was also increased in the same fraction of frontal cortex (+24.2%) and in the striatum (+45.9%), although in this last area the mechanism appeared to be different because the proteinlevel of the kinase was also markedly increased (+43.7%). However, the effect of treatment was not restricted to the presynaptic kinase, because CaMKII activity was also increased in the total cellular cytosol in cortical areas. The autonomous (calcium-independent) activity of CaMKII was assayed for the first time after antidepressant treatment, and found to be increased in synaptic vesicles of all three areas. These results confirmed the involvement of CaMKII in antidepressant drug action and suggested that modulationof transmitter release is a primary component in the action of psychotropic drugs. (C) 2000 American College of Neuropsychopharmacology. Published byElsevier Science Inc.

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Documento generato il 23/01/20 alle ore 03:36:18