It is well established that ginseng saponin has positive influences on vari
ous neural diseases, but little is known about its electrophysiological eff
ects in the central nervous system. In this study, we examined the electrop
hysiological effects of ginseng saponin in rat hippocampal slices, Total sa
ponin from ginseng root reduced the slope of fEPSPs (field excitatory posts
ynaptic potentials) in the CA1 area in a dose-dependent manner (9.1 +/- 5.4
%, 48.4 +/- 12.1%, and 60.5 +/- 15.3% at 10, 50, and 100 mu g/ml, respectiv
ely), which was reversed within 10 min of washout. Seven different ginsenos
ides resulted in varied degrees of fEPSPs reduction, The rank order of redu
ction was Rb1, Rg1 > Rg2, Rh1, Rc > Rd, Re within a range of 5-64% reductio
n, No difference in the suppressive action between protopanasadiol (Rb1, Rc
, Rd) and protopanaxatriol (Rg1, Rg2, Re, Rh1) saponins was shown; the slop
e of fEPSPs was reduced by 38% and 40% on average, respectively. The possib
le role of gamma-aminobutyric acid (GABA(A)) receptor in the suppressive ac
tion of ginseng saponins was tested using whole cell patch recording in acu
tely isolated hippocampal neurons, Ginsenosides did not induce chloride cur
rent nor modified GABA-induced current, Also, the suppressive effect of gin
senosides on fEPSPs was still observed in the presence of the GABA(A) recep
tor antagonist, bicuculline methiodide 50 mu M. These results suggest that
the suppressive effect is not attributable to regulation of GABA(A) recepto
r activation.