Vinpocetine Selectively Inhibits Neurotransmitter Release Triggered by Sodium Channel Activation

摘要: The effects of vinpocetine on internal Na+ (Nai), cAMP accumulation, Ca2+ (Cai) and excitatory amino acid neurotransmitters release, under resting depolarized conditions, was investigated in rat striatum synaptosomes. Veratridine (20 μM) or high K+ (30 mM) were used as depolarizing agents. Results show that the low μM range inhibits elevation Nai, Cai release glutamate aspartate induced by veratridine depolarization. In contrast, fails to inhibit rise neurotransmitter K+, which are both TTX insensitive responses. also inhibition exerted all above veratridine-induced responses is not reflected PDE activity. Our interpretation these results triggered activation voltage sensitive channels, but a direct VSCC. Thus, main mechanism involved neuroprotective action CNS unlikely be due channels enzymes, rather presynaptic channel-activation unchained