Abstract
The purpose of this study was to investigate different forms of long-term potentiation (LTP) induced by different compounds. As shown in results, the influx of calcium via voltage-dependent calcium channels (VDCCs) was responsible for ( − )-clausenamide-induced LTP in hippocampus, while Rg1 induced LTP is mediated by the entry of calcium via N-methyl-d-aspartate glutamate (NMDA) receptor. The findings in the present study provide pharmacological basis for the nootropic mechanisms of these two compounds.
Notes
‡ Current address: Clinical Psychopharmacology Section, National Institute on Drug Abuse, National Institutes of Health, Baltimore, 333 Cassell Drive, Baltimore, MD 21224, USA.
¶ Current address: Department of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn Street, Baltimore, MD 21201, USA.