Lithium-induced activation of Akt and CaM kinase II contributes to its neuroprotective action in a rat microsphere embolism model.
Brain Res
; 1108(1): 98-106, 2006 Sep 07.
Article
em En
| MEDLINE
| ID: mdl-16843447
ABSTRACT
Lithium used in bipolar mood disorder therapy protects neurons from brain ischemic cell death. Here, we documented that lithium administration under microsphere-embolism (ME)-induced brain ischemia restored decreased protein kinase B (Akt) and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activities 24 h after ischemia in rat brain. Akt activation was associated with increased phosphorylation of its potential targets forkhead transcription factor (FKHR) and glycogen synthase kinase-3beta (GSK-3beta). In parallel with decreased CaMKII autophosphorylation, we also found marked dephosphorylation of tau proteins 24-72 h after ME. Increased protein phosphatase 2A (PP2A) activity was found 24 h after ME. Inhibition of increased PP2A activity by lithium treatment apparently mediated restored tau phosphorylation. Taken together, activation of Akt and CaMKII by lithium was associated with neuroprotective activity in ME-induced neuronal injury.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Isquemia Encefálica
/
Cloreto de Lítio
/
Proteínas Quinases Dependentes de Cálcio-Calmodulina
/
Infarto Encefálico
/
Proteínas Proto-Oncogênicas c-akt
Tipo de estudo:
Prognostic_studies
Idioma:
En
Revista:
Brain Res
Ano de publicação:
2006
Tipo de documento:
Article
País de afiliação:
Japão