Large multipolar interneurons (LMI) are suspected to underlie a lateral inhibition onto the granular layer of ELL when stimulated by distal mormyromast afferents from the skin (Han, Grant, and Bell, 2000). It is unknown what role, if any, these cells play at the level of a single afferent to granular cell relay (when only a single afferent fiber is stimulated, and lateral inhibition is assumed to be inactive). However, the presence of a large LMI calyx onto the somata of ELL granular cells, as well as the possibility of undocumented synapses between the juxtalobar input and LMI somata (Meek, Grant and Bell, 1999), provided sufficient rationale for inclusion of variably controlled IPSPs in permutations of this model.

Although a model describing ephaptic excitation of the LMI presynaptic terminal (caused by extracellular K⁺ accumulation following granular cell depolarization) in a biologically realistic manner was not included in this model, it was possible to arbitrarily apply realistic GABA_A mediated IPSPs to the model granular cell. When included, the timing of these IPSPs was determined either by the constraint of burst offset at an experimentally suggested post-EOCD latency, or by a hypothetical network scheme involving approximation of ephaptic excitation by a fast AMPA-type synapse. IPSPs were modeled similarly to the AMPA-mediated EPSPs described above, with t _decay times ranging between 3 and 15ms (Gabbiani et al., 1994) and a reversal potential of —65mV (set to resting potential for sake of simplicity).