Inactivation of GABA(A) receptor reduces ginsenoside Rb3 neuroprotection in mouse hippocampal slices after oxygen-glucose deprivation.

To investigate the effect of ginsenoside Rb(3) on synaptic transmission after oxygen-glucose deprivation in vitro. The population spike (PS) was recorded in the stratum pyramidale of mouse hippocampal slices using extracellular recordings. Ginsenoside Rb(3) depressed the basal synaptic transmission, which also promoted the recovery amplitude of PS after OGD in a concentration-dependent manner. The GABA(A) receptor agonist muscimol improved the recovery, which was similar to that of ginsenoside Rb(3). Moreover, the effect of ginsenoside Rb(3) in combination with muscimol was not additive. Treatment with the GABA(A) receptor antagonist bicuculline or picrotoxin, which prevented the depression of PS caused by ginsenoside Rb(3), also reduced the neuroprotection. The results indicate that the activation of the GABA(A) receptor is correlated with the neuroprotective mechanisms of ginsenoside Rb(3).