Affiliation:
1. Department of Physiology, School of Medicine, Universidad Nacional Autónoma de México (UNAM), Apdo. Postal 70-250, C.P. 04510, México, D.F., México
Abstract
No mechanistic actions for piracetam have been documented to support its nootropic effects. Voltage-gated calcium channels have been proposed as a promising pharmacological target of nootropic drugs. In this study, we investigated the effect of piracetam on CaV2.2 channels in peripheral neurons, using patch-clamp recordings from cultured superior cervical ganglion neurons. In addition, we tested if CaV2.2 channel inhibition could be related with the effects of piracetam on central neurons. We found that piracetam inhibited native CaV2.2 channels in superior cervical ganglion neurons in a dose-dependent manner, with an IC50 of 3.4 μmol/L and a Hill coefficient of 1.1. GDP βS dialysis did not prevent piracetam-induced inhibition of CaV2.2 channels and G-protein-coupled receptor activation by noradrenaline did not occlude the piracetam effect. Piracetam altered the biophysical characteristics of CaV2.2 channel such as facilitation ratio. In hippocampal slices, piracetam and ω-conotoxin GVIA diminished the frequency of excitatory postsynaptic potentials and action potentials. Our results provide evidence of piracetam's actions on CaV2.2 channels in peripheral neurons, which might explain some of its nootropic effects in central neurons.
Subject
General Biochemistry, Genetics and Molecular Biology
Cited by
5 articles.
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