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Calcium-dependent prevention of neuronal apoptosis by lithium ion: essential role of phosphoinositide 3-kinase and phospholipase Cgamma.

Authors
Kang, HJ; Noh, JS; Bae, YS; Gwag, BJ
Citation
Molecular pharmacology, 64(2):228-234, 2003
Journal Title
Molecular pharmacology
ISSN
0026-895X1521-0111
Abstract
We examined the possibility that the neuroprotective effects of Li+ would depend upon the patterns of neuronal death, apoptosis versus necrosis, and whether Ca2+ as well as phosphoinositide 3-kinase (PI3-K) would mediate the neuroprotective effect of Li+. Cortical neurons treated with Li+ showed marked increase in [Ca2+]i within 2 min. Addition of BAPTA-acetoxymethyl ester, a selective Ca2+ chelator, abrogated the antiapoptotic effect of Li+. PI3-K was activated rapidly within 1 min after exposure to Li+, which mediated Ca2+-dependent neuroprotective effects of Li+. Activated PI3-K seemed to increase [Ca2+]i via the phospholipase Cgamma (PLCgamma) pathway. Antiapoptosis action of Li+ was prevented in the presence of U-73122, a selective phospholipase C inhibitor, and was not observed in PLCgamma1-null fibroblasts. In contrast to antiapoptosis action, administration of Li+ did not prevent neuronal cell necrosis by excitotoxicity or free radicals. Li+ selectively prevents apoptosis by increasing [Ca2+]i through activation of PI3-K and PLCgamma pathways.
MeSH terms
AnimalsApoptosis*Calcium/antagonists & inhibitorsCalcium/pharmacology*Drug InteractionsHumansLithium/pharmacology*MiceMice, Inbred ICRNeurons/cytologyNeurons/drug effects*Phosphatidylinositol 3-Kinases/physiology*Phospholipase C gammaType C Phospholipases/physiology*
DOI
10.1124/mol.64.2.228
PMID
12869627
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
Journal Papers > School of Medicine / Graduate School of Medicine > Psychiatry & Behavioural Sciences
AJOU Authors
노, 재성곽, 병주
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