Fig. 11.
The PP was associated with a largeRIN decrease and could not be terminated by hyperpolarizing pulses. A, Cholinergic-dependent PPs illustrated on two time scales. In the latter, brief current injection (−50 pA; 0.2 sec; 0.5 Hz) demonstrated a large decreasedRIN. B, PPs in the presence of carbachol, TTX, and K+ channel blockers (10 mm TEA, 5 mm 4-AP, 100 μm Ba2+). Under these conditions, brief current injection confirmed anRIN decrease in the absence of slow Na+ oscillations and suppression of K+ channels. C, A graph depicting the decreased RIN relative to control obtained at the resting potential, versus duration of the PP. In the same graph, membrane potential was also plotted versus PP duration. BothRIN and membrane potential values were obtained from the neuron illustrated in B (*). Notice that the change in membrane potential was minimal, whereas the increase inRIN was significant. D, Two superimposed PPs evoked from a CA1 pyramidal neuron. In the broken trace, hyperpolarizing current injection (−0.4 nA; 0.8 sec) failed to terminate the PP.