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. Author manuscript; available in PMC: 2018 Sep 1.
Published in final edited form as: Endocrinology. 2008 Mar 27;149(7):3598–3604. doi: 10.1210/en.2007-1631

Figure 2. SK channels restrain the excitability of GnRH neurons.

Figure 2

A, representative voltage trace of a silent GnRH neuron at rest membrane potential showing apamin-induced depolarization and firing. Filled squares and open circles indicate the pre- and post-, respectively, responses evoked by depolarizing current injections of 2 seconds (from 5 to 30pA, increment of 5pA). B, plot of number of action potentials induced by 2 s depolarizing currents as a function of amplitude of injection currents before and immediately after apamin treatment as indicated in A. C, a representative voltage trace of a spontaneously active, non-bursting cell responding to apamin with a small depolarization and increase in firing frequency. D, histogram showing effect of apamin on firing frequency of cell in C. E, representative voltage trace of a spontaneously-active bursting GnRH neuron in which apamin evokes depolarization and increased burst firing. F, plot of current induced by voltage ramp from -120 to -40mV in cell shown in E, before (left arrow E) and after apamin (right arrowhead E), as a function of holding potentials. The dashed line shows the apamin-induced current obtained by subtraction of currents before and immediately after apamin treatment. G, representative voltage trace of apamin-evoked depolarization in the presence of TTX, kynurenic acid (1 mM) and picrotoxin (0.1 mM). H, histogram summarizing the apamin-evoked depolarization in the absence and presence of TTX (0.5 μM), kynurenic acid (1 mM) and picrotoxin (0.1 mM). Note that the large upward and downward deflections on the traces are responses to the injection of hyperpolarizing or depolarizing currents to test membrane resistance.