Figure 8. A gap junction inhibitor enhances activity-dependent depolarizing shifts in the E_IPSC.

A, recordings of GABA_A receptor-mediated postsynaptic currents in a CA1 pyramidal neuron evoked by tetanus stimulation (50 Hz, 2 s) to the SLM before and after perfusion of octanol (1 mm). Traces were low-pass filtered at 40 Hz to reduce stimulus artefacts. Traces were recorded with various holding potentials from −30 to −80 mV (10 mV decrement) with a 1 min interval and the baselines were superimposed. The I–V relationship after the second stimulus (early phase; indicated by the dashed lines and open circles) and the 90th stimulus (late phase; indicated by the continuous lines and filled circles) are plotted from each trace. Blue and red lines indicate before and after octanol perfusion, respectively. Note that octanol shifted the E_IPSC in the late phase of tetanus but not in the early phase. The inset shows IPSCs evoked by paired stimuli in the same cell, which were not altered by octanol. B, means ±s.e.m. of the E_IPSC in the early (○) and late phase (•). C, the change in E_IPSC from that of the second stimulus (ΔE_IPSC) plotted after every five stimulations. Octanol significantly enhanced the ΔE_IPSC in the later phase of tetanus stimulation. *P < 0.05; N.S., not significant.