Abstract: Abstract: Objective To study the underling mechanism of the effect of ginsenosides(GS) on spontaneous sleep. Methods Adult SD rats were randomly divided into the control, GS 10 mg/kg (low dose) and 100 mg/kg (high dose) groups. Rats were instrumented with sleep-wake recording electrodes. After recovery from surgical operation, rats were orally administered GS 10 mg/kg and 100 mg/kg or water once per day for 6 days. On GS administration day 1 and day 6, Polygraphic signs of undisturbed sleep-wake activities were recorded for 12h (7:30 ~19:30) after GS administration. Results On GS administration day 1 (acute), 10 mg/kg GS slightly (P?>0.05 but 100mg/kg GS significantly (P?<0.05) increased the non-rapid eye movement (NREM) and total sleep and decreased wakefulness; compared with control, low dose and high dose GS failed to change the level of glutamic acid decarboxylase (GAD) (P?>0.05) but enhanced the expressions of GABAA receptor α,? not ? subunits in rat hypothalamus (P?<0.05). Following 6 days administration (chronic), both 10 and 100mg/kg GS increased markedly NREM and total sleep and decreased wakefulness. Accordingly, low dose GS slightly (P?>0.05) but high dose GS significantly (P? <0.05) increased the level of GAD in rat hypothalamus, whereas the expressions of GABAA receptor α, ? and ? subunits not affected (P?>0.05). Conclusion These results suggest that GS can regulate spontaneous sleep architecture in time and dose-dependent manner in which acute GS treatment is related to its up-regulating GABAA receptor α, ? subtypes whereas chronic GS administration involved in the raised GABA product produced by its over-expressing GAD in rat hypothalamus.

Key words: Ginsenosides, rapid eye movement sleep, non rapid eye movement sleep, electroencephalogram, GABAA receptor