Neuroprotective Effects of Lithium on NMDA-induced Excitotoxicity in Mouse Cerebrum
The Korean Journal of Physiology and Pharmacology
;
: 111-121, 2006.
Article
in English
| WPRIM
| ID: wpr-728570
ABSTRACT
Neuroprotective properties of lithium were evaluated by using in vivo NMDA excitotoxicity model. Systemic injection of NMDA to young mice induced neuronal apoptosis mediated by both TNFR-1 and Fas ligand, and long-term lithium treatment showed noticeable neuroprotection against NMDA-induced excitotoxicity NMDA-damaged neurons expressed several apoptosis-related gene products such as TNFR-1, Fas ligand, and caspase-3, and these gene expressions were not found in the brain of mice chronically treated with lithium. Therefore, it is highly likely that the protection offered by chronic lithium treatment occurred at far upstream of caspase activation, since the chronic lithium treatment increased the expression of Bcl-2, an important antiapoptotic gene known to act upstream of caspase cascade. Timm's histochemistry indicated the complete blockade of the NMDA insults by the treatment. There was no indication of axonal regeneration, which follows synaptic degeneration induced by neuronal damage. Furthermore, this study reports for the first time that TNFR-1 and Fas ligand are involved in neuroprotective effects of lithium in NMDA-induced neuronal apoptosis.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Regeneration
/
Axons
/
Brain
/
Gene Expression
/
N-Methylaspartate
/
Apoptosis
/
Neuroprotective Agents
/
Caspase 3
/
Fas Ligand Protein
/
Cerebrum
Type of study:
Prognostic study
Limits:
Animals
Language:
English
Journal:
The Korean Journal of Physiology and Pharmacology
Year:
2006
Type:
Article
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