Model 1a, Bursting Properties
Delay between EOCD and primary afferent inputs was varied between 0 and 6ms, producing model granular cell bursts containing between 6 and 0 spikes, respectively (figure 6). The temporal sensitivity of this response roughly matched experimental results from the previously described extracellular field recordings (figure 2b, figure 6; Bell and Grant, 1992). As shown in voltage traces from NEURON, the first spike in the burst is of a greater amplitude (~60mV) than subsequent spikes (~40mV) for delays of less than 2ms (figure 8). Spike attenuation during the burst was minimal, and action potential shape (upstroke, width, and afterhyperpolarization) remained relatively homogenous during the burst. Increasing the delay to more than 1ms decreased the degree to which the two inputs initially summated so that spike threshold was reached gradually via subthreshold I-NaP activation. At a delay of 6ms, this persistent Na+ channel amplification was insufficient to reach spike threshold before arrival of the LMI IPSP, and the granular cell membrane potential gradually returned to resting without having produced a spike. However, the hyperpolarizing inflection at ~52ms post-EOCD, due to I-KA activation, indicates that spike threshold was very nearly reached at a delay of 6ms.
