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OBJECTIVE Insomnia is an extremely common symptom in modern society.We have demonstrated that YZG-330 which is a new modifier of N6-(4-hydroxybenzyl) adenine riboside can enhance pentobarbital-induced sleep behaviors.In this study, in order to investigate the mechanism of this action, we measured the chloride (Cl-) flux in primary cultured cerebellar granule cells.METHODS Primary cultures of cerebellar cells were prepared from the cerebelli of 7-8-old mice.Neurons were used for Cl-perme-ability experiments 8-10 d after preparation.We used the chloride-sensitive fluorescent probe N-(ethoxycarbonylmethyl)-methoxyquinolinium bromide (MQAE) as a tool to estimate the effect of GABA (100 μmol·L-1 and 300 μmol·L-1) and YZG-330 (10 μmol·L-1 and 1 μmol· L-1) on GABAA receptor function.And we used picrotoxin (100 μmol· L-1 and 10 μmol· L-1) to observe whether it can antagonize the effect of YZG-330 (10 μmol·L-1 and 1 μmol· L-1) on chloride flux.RESULTS The rate of chloride flux for GABA (300 μmol· L-1 and 100 μμmol· L-1) were increased * to 214% and 181% of control respectively, and the rate of chloride flux for YZG-330 (10 μmol·L-1 and 1 μmol·L-1) were increased to 177% and 150% of control respectively.Picrotoxin (100 μ mol·L-1) partly blocked YZG-330 (1 μmol·L-1)-enhanced chloride flux, and the inhibition rate was 36%.CONCLUSION These data indicate that the effect of chloride flux stimulated by YZG-330 may be mediated by GABAA receptor activation.