Abstract
Treatment with ginsenosides attenuated KA-induced seizures and oxidative stress in the synaptosome, and reduced synaptic vesicles at the presynaptic terminals dose-dependently. The adenosine A2A receptor antagonist 1,3,7-trimethyl-8-(3-chlorostyryl) xanthine reversed the ginsenoside-mediated pharmacological actions. Neither the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine nor the adenosine A2B receptor antagonist alloxazine affected the ginsenoside-mediated pharmacological actions. Our results suggest that ginsenosides block KA-induced synaptosomal oxidative stress, associated with hippocampal degeneration, through activation of adenosine A2A receptors.
Original language | English |
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Pages (from-to) | 239-245 |
Number of pages | 7 |
Journal | Behavioural Brain Research |
Volume | 197 |
Issue number | 1 |
DOIs | |
Publication status | Published - 2009 Jan 30 |
Keywords
- Adenosine A receptor
- Ginsenosides
- Hippocampus
- Kainate
- Oxidative stress
- Synaptosome
ASJC Scopus subject areas
- Behavioral Neuroscience