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Abstract-Pharmacological studies of neutral saponins (GNS) of Panax Ginseng root, were performed.GNS showed CNS-depressant action in inhibition of spontaneous and exploratory movements, and in potentiation of CNS-depressant.A specific blocking action of conditioned response by GNS was significantly confirmed in small doses and did not produce loss of righting reflex, motor incoordination or myorelaxation.Analgesic, anticonvulsant and antipyretic effects were recognized. From the tests described above in addition to those of traction, hypothermia, fighting behavior and ratio of two reflexes, GNS appears to have neuroleptic activity. There was neither hemolytic nor vasodilator action on the hind leg or coronary vascular beds.It is said that the Chinese medicine Ginseng root has some effect on the central nervous system and several reports concerning neuropharmacological properties of Ginseng root have so far been published (1-7). Stimulant action was proved by Brekhman and his co-workers with mice swimming in water (1), and running up an endless rope (2). Petkov (7) also reported the stimulant effect of water-alcohol extracts on the central nervous system and analeptic activity, while on the contrary, antialarm action has also been reported (3-6).In our laboratory, a number of relatively simple tests were employed to obtain a pharmacological spectrum of the activity of extracts, which had been supplied from Shibata et al. (8). From these results, a crude saponin fraction (G. NO. 3) and GNS, a mixture of neutral saponins, were estimated as having neuroleptic activity (9, 10).The present study is an attempt to investigate neuroleptic properties of GNS. MATERIALS AND METHODSGNS is a mixture of neutral saponins mainly composed of Ginsenoside-Rb1, -Rb2and -Rc. Details of the separation have been described by Shibata et al. (8). The solution of GNS was prepared with physiological saline with the following methods being employed :1) Acute toxicity in mice Male mice (ddy-strain), weighing 18-21 g, were used and the intravenous, intraperitoneal and oral LD,,, were determined. Mortality was recorded 72 hr after administration. Intraperitoneal and oral LD50 were calculated by the method of Behrens-Karber (11). Intravenous LD50 was done by the up and down method.

Abstract-Toclarify the relation between the negative inotropic effects of "calcirun antagonistic" vasodilators and their calcium-antagonistic effects,

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