Calcium-dependent prevention of neuronal apoptosis by lithium ion: Essential role of phosphoinositide 3-kinase and phospholipase C gamma
- Authors
- Kang, Hyo Jung; Noh, Jai Sung; Bae, Yun Soo; Gwag, Byong Joo
- Issue Date
- Aug-2003
- Publisher
- AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
- Citation
- MOLECULAR PHARMACOLOGY, v.64, no.2, pp 228 - 234
- Pages
- 7
- Journal Title
- MOLECULAR PHARMACOLOGY
- Volume
- 64
- Number
- 2
- Start Page
- 228
- End Page
- 234
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/36715
- DOI
- 10.1124/mol.64.2.228
- ISSN
- 0026-895X
1521-0111
- 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.
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Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
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