Active electrolocation in Gnathonemus petersii requires a temporally precise neural mechanism of encoding both stimulus presence and stimulus intensity. In the first case, efferent gating of sensory inputs by the EOCD enhances only those inputs that arrive within a certain time window with respect to the expected arrival of the fish’s EOD at cutaneous mormyromast receptors. In the second case, stimulus intensity is initially coded by the latency to fire of mormyromast receptors. Object location and distance from the fish are then calculated by comparing the amplitude and slope of the electrical image on the skin. Preservation of information enabling these calculations requires a transformation from latency coding to burst duration coding at the granular cell layer of the medial ELL, which receives inputs from mormyromast primary afferents, the juxtalobar nucleus, and large multipolar inhibitory neurons that are known to be activated by electrical stimulation of distal skin areas.

Modeling results of this study show that the transformation from primary afferent latency to burst duration in the granular cell layer can be almost completely explained by the interaction of a pair of putative, noninactivating Na⁺ and K⁺ ion channel conductances. Although restriction of burst offset times to experimentally described ranges was only accomplished by incorporation of previously undocumented LMI interactions at the level of single afferent fiber stimulation, it is conceivable that the gating kinetics of modeled ionic currents differ from granular cell currents in vivo and that this could alleviate the need for LMI recruitment. This second possibility is suggested by the ability of models 2a and 2b to retain the hypothesized coding transformation, despite the poor fit of burst offset latency for these models.

Since the full physiologically relevant range of delays between arrival of EOCD and primary afferent inputs to the granular cell appears to be around 6ms, and, furthermore, the granular cell is known to be electrotonically compact and therefore relatively homogenous in terms of input and integrative geometries, the generation of bursts of variable duration must depend entirely on amplification of the intitial difference of summated depolarization following these two inputs. Two well described mechanisms for such EPSP amplification are the NMDA receptor and the persistent inward Na⁺ current, I-NaP.

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