Neuroprotection of lithium is associated with inhibition of Bax expression and caspase 8 activation.
- Author:
Gee youn KWON
1
;
Soo kyung KIM
Author Information
1. Department of Pharmacology, School of Medicine, Keimyung University, 194 Dongsan-dong, Chung-gu, Daegu, 700-712, South Korea. green@dsmc.or.kr
- Publication Type:Original Article
- MeSH:
Animals;
Caspase 8*;
Cerebrum;
Hippocampus;
In Situ Nick-End Labeling;
Lithium*;
Mice;
N-Methylaspartate;
Thalamus
- From:The Korean Journal of Physiology and Pharmacology
2001;5(5):389-396
- CountryRepublic of Korea
- Language:English
-
Abstract:
Neuroprotective properties of lithium were investigated by using in vivo NMDA excitotoxicity model. The appearance of TUNEL positive cells was prominent within 24 h of NMDA (70 mg/kg, i.p.) injection in the regions of the cortex, hippocampal formation, and thalamus of mouse cerebrum. NMDA treatment resulted in the extensive enhancement of Bax immunoreactivity in the cortical and hippocampal regions. NMDA also increased the immunoreactivity of caspase 8 in the similar regions of the mouse cerebrum. However, the increased immunoreactivity of Bax and caspase 8 were dramatically attenuated by chronic lithium pretreatment (lithium chloride, 300 mg/kg/d, i.p. for 7-10 days). At the same time, lithium ion blocked the appearance of TUNEL positive cells, and the morphological assessment indicated an effective neuroprotection by lithium against NMDA excitotoxicity. Although the exact action mechanism of lithium is not straightforward at this time, we propose that the inhibition of Bax and caspase cascade is involved in the neuroprotective action of lithium.
