Effects of the ginsenosides Rg1 and Rb1 on morphine-induced hyperactivity and reinforcement in mice

• Published in: Journal of pharmacy and pharmacology Vol. 50; no. 5; p. 555
• Main Authors: Kim, H S, Hong, Y T, Jang, C G
• Format: Journal Article
• Language: English
• Published: England 01.05.1998
• Subjects: Animals; Central Nervous System Agents - pharmacology; Drug Interactions; Ginsenosides; Hyperkinesis - chemically induced; Hyperkinesis - drug therapy; Hyperkinesis - prevention & control; Male; Mice; Mice, Inbred ICR; Morphine - antagonists & inhibitors; Morphine - pharmacology; Motor Activity - drug effects; Saponins - pharmacology
• ISSN: 0022-3573
• DOI: 10.1111/j.2042-7158.1998.tb06198.x

Recent studies have demonstrated that ginseng saponin inhibits the hyperactivity and conditioned place-preference response induced by psychostimulants and opiates. This seems to occur by direct or indirect modulation of dopaminergic activity. However, it is not known which components of ginseng saponin are active. These experiments were conducted to determine the effects of the ginsenosides Rb1 and Rg1, major components of the protopanaxadiol and protopanaxatriol fractions of ginseng saponin, on morphine-induced hyperactivity and conditioned place-preference. Morphine-induced hyperactivity, but not apomorphine-induced climbing behaviour, was inhibited by both Rb1 and Rg1. These findings confirm the hypothesis that ginsenosides modulate catecholaminergic activity preferentially at pre-synaptic sites. Morphine-induced conditioned place-preference was inhibited by Rg1, but not by Rb1. It has previously been shown that at low doses Rb1 and Rg1 are equally effective at inhibition of catecholamine secretion at the pre-synaptic site, but that at high doses Rg1 is a more effective inhibitor. This observation might explain our finding that morphine-induced conditioned place-preference was inhibited by Rg1 only. Our findings suggest that Rg1, a component of ginseng saponin with appropriate activity, might be a useful agent for prevention and treatment of the adverse effects of morphine.