Spike waveforms in the HH model with varied BK.

<p><b>(A)</b> shows the voltage, <i>I</i><sub>BK</sub> current, and <i>I</i><sub>BK</sub> activation behaviour of a spike induced by a 5-nA current step for 5 ms, in the original oxytocin HH model (yellow, τ<sub>pd</sub> = 1.22 ms), and the adjusted model (green; τ<sub>pd</sub> = 10 ms). Experimentally, the HAP lasts for 25–125 ms and hyperpolarises the cell by ~7.5 mV [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0180368#pone.0180368.ref018" target="_blank">18</a>]. In the original HH model, the HAP is too short and too small, because <i>I</i><sub>BK</sub> both rises and falls sharply after a spike. In the adjusted model, <i>I</i><sub>BK</sub> is prolonged by the slower deactivation, making a better match to the HAP observed <i>in vitro</i>, as well as improving the fit to the <i>in vivo</i> ISI distribution. <b>(B)</b> shows, for the adjusted model, the effects of setting <i>g</i><sub>BK</sub> = 0 (red, compared to original value <i>g</i><sub>BK</sub> = 1, in green), on a single spike induced by an 8-nA current step for 3 ms, to simulate the pharmacological block of <i>I</i><sub>BK</sub> [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0180368#pone.0180368.ref018" target="_blank">18</a>]. When <i>I</i><sub>BK</sub> is blocked, the HAP is smaller and decays faster. <b>(C)</b> shows the <i>in vitro</i> experiment data simulated in (B), redrawn from [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0180368#pone.0180368.ref018" target="_blank">18</a>]. The duration and amplitude of the HAP is a much closer match to the adjusted model. The block shows only a partial reduction, but is likely to be less total than the model.</p>