Skip to main content
. 2015 May 11;40(1):55–61. doi: 10.1016/j.jgr.2015.05.001

Fig. 2.

Fig. 2

Oral administration of gintonin enhances long-term synaptic potentiation in the Shaffer collateral pathway. (A) Theta burst stimulations (TBS, 20 bursts of 4 pulses at 100 Hz) were given at CA3-CA1 synapses from acutely prepared hippocampal slices after daily oral administration of vehicle or gintonin for 7 d (50 mg/kg). (B) In the gintonin-administered group, both the rise slope (10–90%) and amplitude of the stimulated pathway were significantly more potentiated than the vehicle-administered group (34% vs. 86% for rise slope, *p < 0.05; 30% vs. 67% for amplitude, **p < 0.01, vehicle vs. gintonin group, respectively, n = 7–17). The bar graph showed the fold change in rise slope and amplitude of 60 min after LTP induction compared to baseline. (C) Stimulated pathways were significantly potentiated after gintonin administration compared to control pathway (gintonin: rise slope, **p < 0.01, amplitude, **p < 0.01, vehicle: rise slope, **p < 0.01, amplitude, *p < 0.05). The gray trace represents an averaged field excitatory postsynaptic potentials (fEPSP) during baseline (a) and the black trace represents an averaged fEPSP response 50–60 min after TBS stimulation (b) (scale bar: 20 ms and 0.2 mV). Error bars represent standard error of the mean.