Jujuboside A (JuA) is a main component of Jujubogenin extracted from the seeds of Ziziphus. The authors have not seen any report on JuA’s direct effect on the neurons of the central nervous system. This study aimed to assess the effect of JuA on paired pulse responses of dentate gyrus granule cells in urethane anaesthetized rats, used intracerebroventricular (i.c.v.) JuA to mimic in vitro bath conditions in vivo. Paired pulse stimuli with 80ms interpulse interval were used to stimulate the perforant pathway. Evoked responses were recorded in the dentate gyrus cell layer after i.c.v. administration of 0.9% normal saline or JuA. In the first responses, the slopes of excitatory postsynaptic potential (EPSP1) and the amplitudes of population spike (PS1) decreased significantly after administration of JuA while the PS1 latencies increased significantly. In the second responses, the EPSP2 slopes and PS2 latencies were changed similarly to those of the first ones, but PS2 amplitudes increased. The results showed that JuA may have some inhibitory effect on the granule cell excitability mediated by presynaptic mechanism but may have little effect on the excitability mediated by postsynaptic mechanism since the second evoked N methyl D aspartic mediating paired pulse facilitation is a postsynaptic mechanism. Jujuboside A (JuA) is a main component of Jujubogenin extracted from the seeds of Ziziphus. The authors have not seen any report on JuA’s direct effect on the neurons of the central nervous system. This study aims to assess the effect of JuA on paired pulse. Responses of dentate gyrus granule cells in urethane anaesthetized rats, used intracerebroventricular (icv) JuA to mimic in vitro bath conditions in vivo. Paired pulse stimuli with 80ms interpulse interval were used to stimulate the perforant pathway. Evoked responses were recorded in the dentate gyrus cell Layer after icv administration of 0.9% normal saline or JuA. In the first responses, the slopes of excitatory postsynaptic potential (EPSP1) and the amplitudes of population spike (PS1) decreased significantly after administration of JuA while the PS1 latencies increased significantly. In the Second responses, the EPSP2 slopes and PS2 latencies were changed similarly to those of the first ones, but PS2 amplitudes increa Sed. The results showed that JuA may have some inhibitory effect on the granule cell excitability mediated by presynaptic mechanism but may have little effect on the excitability mediated by postsynaptic mechanism since the second evoked N methyl D aspartic mediating paired pulse facilitation is a postsynaptic mechanism.