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Abstract Synaptic and neural properties can change during periods of auditory deprivation. These changes may disrupt the computations that neurons perform. In the brainstem of chickens, auditory deprivation can lead to changes in the size and biophysics of the axon initial segment (AIS) of neurons in the sound source localization circuit. This is the phenomenon of axon initial segment (AIS) plasticity. Individuals who use cochlear implants (CIs) experience periods of hearing loss, and so we ask whether AIS plasticity in neurons of the medial superior olive (MSO), a key stage of sound location processing, would impact time difference sensitivity in the scenario of hearing with cochlear implants. The biophysical changes that we implement in our model of AIS plasticity include enlargement of the AIS and replacement of low-threshold potassium conductance with the more slowly-activated M-type potassium conductance. AIS plasticity has been observed to have a homeostatic effect with respect to excitability. In our model, AIS plasticity has the additional effect of converting MSO neurons from phasic firing type to tonic firing type. Phasic firing is known to have greater temporal sensitivity to coincident inputs. Consistent with this, we find AIS plasticity degrades time difference sensitivity in the auditory deprived MSO neuron model across a range of stimulus parameters. Our study illustrates a possible mechanism of cellular plasticity in a non-peripheral stage of neural processing that could impose barriers to sound source localization by bilateral cochlear implant users. 

Locomotion generates adventitious sounds which enable detection and localization of predators and prey. Such sounds contain brisk changes or transients in amplitude. We investigated the hypothesis that ill-understood temporal specializations in binaural circuits subserve lateralization of such sound transients, based on different time of arrival at the ears (interaural time differences, ITDs). We find that Lateral Superior Olive (LSO) neurons show exquisite ITD-sensitivity, reflecting extreme precision and reliability of excitatory and inhibitory postsynaptic potentials, in contrast to Medial Superior Olive neurons, traditionally viewed as the ultimate ITD-detectors. In vivo, inhibition blocks LSO excitation over an extremely short window, which, in vitro, required synaptically evoked inhibition. Light and electron microscopy revealed inhibitory synapses on the axon initial segment as the structural basis of this observation. These results reveal a neural vetoing mechanism with extreme temporal and spatial precision and establish the LSO as the primary nucleus for binaural processing of sound transients.