Inhibitory effects of jujuboside A on EEG and hippocampal glutamate in hyperactive rat

In this study, the inhibitory effect of jujuboside A (JuA) on a penicillin sodium (Na-PCN) induced hyperactivity model was investigated. Cortical EEG (electroencephalogram) and the concentration of hippocampal Glutamate (Glu) were monitored simultaneously in vivo as indicators of rat’s excitatory state. Power spectral density (PSD) and gravity frequency of PSD were calculated. JuA (0.05 g/L and 0.1 g/L) inhibited the EEG excitation effect caused by Na-PCN by increasing the power of δ1 and δ2 bands (P<0.01 vs model) and lowering the gravity frequency of PSD (P<0.01 vs model). JuA also remarkably reduced the Glu elevation induced by Na-PCN (P<0.05 vs model). Diazepam also depressed Glu concentration and lowered the gravity frequency, but it showed a different EEG pattern in increased β2-activity (P<0.01 vs model). EEG excitation caused by Na-PCN correlated with Glu elevation during the first hour. Neurophysiological inhibitory effects of JuA and diazepam were more persistent than their Glu inhibitoty effects.

The effect of Jujuboside A on the evoked field potentials of Granule cells in dentate gyrus

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.