8-(3-chlorostyryl)caffeine and Seizures

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 A(2A) receptor antagonist 1,3,7-trimethyl-8-(3-chlorostyryl) xanthine reversed the ginsenoside-mediated pharmacological actions. Neither the adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine nor the adenosine A(2B) 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 A(2A) receptors.

Topics: Adenosine A2 Receptor Antagonists; Analysis of Variance; Animals; Caffeine; Dose-Response Relationship, Drug; Drug Interactions; Excitatory Amino Acid Agonists; Ginsenosides; Hippocampus; Kainic Acid; Male; Nerve Degeneration; Neuroprotective Agents; Oxidative Stress; Presynaptic Terminals; Rats; Rats, Sprague-Dawley; Seizures; Statistics, Nonparametric; Synaptosomes