Inhibition of nicardipine on amygdala kindling in rats
Abstract
Aim: To investigate the effects and mechanism of nicardipine, a calcium channel blocker, on amygdala kindling in rats.
Methods: Constant current stimulations were delivered to the right amygdala of the rats once a day. The effects of nicardipine on the development and seizure of amygdala kindling were observed and the content of amino acid neurotransmitters in the brain of kindled rats was determined.
Results: Nicardipine (2 mg . kg-1, ip) significantly retarded the development of amygdala kindling (P < 0.01); 2 - 20 mg . kg-1 of nicardipine inhibited amygdala kindled seizure dose-dependently, elevated the afterdischarge threshold, and reduced the Racine's stage; 20 mg . kg-1 of nicardipine significantly increased the content of GABA, a kind of inhibitory amino acid neurotransmitter, in the brain of amygdala kindled rats (P < 0.05).
Conclusion: Nicardipine inhibits amygdala kindling in rats, and the inhibition mechanism may be related to the blockage of the voltage-operated calcium channels and the enhancement of GABAergic system action in the brain.
Keywords:
Methods: Constant current stimulations were delivered to the right amygdala of the rats once a day. The effects of nicardipine on the development and seizure of amygdala kindling were observed and the content of amino acid neurotransmitters in the brain of kindled rats was determined.
Results: Nicardipine (2 mg . kg-1, ip) significantly retarded the development of amygdala kindling (P < 0.01); 2 - 20 mg . kg-1 of nicardipine inhibited amygdala kindled seizure dose-dependently, elevated the afterdischarge threshold, and reduced the Racine's stage; 20 mg . kg-1 of nicardipine significantly increased the content of GABA, a kind of inhibitory amino acid neurotransmitter, in the brain of amygdala kindled rats (P < 0.05).
Conclusion: Nicardipine inhibits amygdala kindling in rats, and the inhibition mechanism may be related to the blockage of the voltage-operated calcium channels and the enhancement of GABAergic system action in the brain.