The quality of visual perception with retinal prostheses strongly depends on the local selectivity. Electrode arrays at the surface of the retina should excite exclusively cells within a local area but they are expected to co-stimulate bypassing axons originating from ganglion cells of the outer regions. Long electrodes parallel to these axons are shown to be good candidates for avoiding the co-stimulation phenomenon. Efficiency of focal excitation depends on the length and resistance of the electrodes.

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Many blind people possess functioning bipolar and ganglion cells, which relay retinal input to the brain. In a two step procedure the excitation of electrically stimulated retinal cells is simulated: (i) the extracellular potential along the neural structure is computed (ii) the target cells are represented by compartment models. Membrane kinetics of the ganglion cells are evaluated with the Fohlmeister-Colman-Miller model. Transmembrane voltages of the bipolar cells are calculated for constant membrane conductance. In retinal ganglion cells the axons are the most excitable structures when stimulated with short cathodic pulses from epiretinal electrodes, whereas the axonal endings are the hot spots in bipolar cells.

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The development of cochlear ilmplants for the treatment of patients with profound hearing loss has advanced considerably in the last few decades, particularly in the field of speech comprehension. However, attempts to provide not only sound decoding but also spatial hearing are limited by our understanding of circuit adaptations in the absence of auditory input. Here we investigate the lateral superior olive (LSO), a nucleus involved in interaural level difference (ILD) processing in the auditory brainstem using a mouse model of congenital deafness (the dn/dn mouse). An electrophysiological investigation of principal neurons of the LSO from the dn/dn mouse reveals a higher than normal proportion of single spiking (SS) neurons, and an increase in the hyperpolarisation-activated Ih current. However, inhibitory glycinergic input to the LSO appears to develop normally both pre and postsynaptically in dn/dn mice despite the absence of auditory nerve activity. In combination with previous electrophysiological findings from the dn/dn mouse, we also compile a simple Hodgkin and Huxley circuit model in order to investigate possible computational deficits in ILD processing resulting from congenital hearing loss. We find that the predominance of SS neurons in the dn/dn LSO may compensate for upstream modifications and help to maintain a functioning ILD circuit in the dn/dn mouse. This could have clinical repercussions on the development of stimulation paradigms for spatial hearing with cochlear implants.