Electrical stimulation of the auditory nerve - III. Response initiation sites and temporal fine structure

Latency, temporal dispersion and input-output characteristics of auditory n erve fiber responses to electrical pulse trains in normal and chronically d eafened cat ears were classified and tentatively associated with sites wher e activity is initiated. Spikes occurred in one or more of four discrete ti me ranges whose endpoints overlapped partially. A responses had latencies < 0.44 ms, exhibited asymptotic temporal dispersion of 8-12 mu s and possess ed an average dynamic range of 1.2 dB for 200 pulses/s (pps) pulse trains. They likely originated from central processes of spiral ganglion cells. B-1 and B-2 responses (0.45-0.9 ms, 25-40 mu s, 1.9 dB) likely stemmed from ac tivity at myelinated and unmyelinated peripheral processes, respectively. C responses (0.9-1.2 ms, > 100 mu s) likely originated from direct stimulati on of inner hair cells, and D responses (> 1.1 ms, > 100 mu s, >8 dB) arose from propagating traveling waves possibly caused by electrically induced m otion of-outer hair cells. C and D responses were recorded only in acoustic ally responsive ears. Mean latencies of spikes in all time ranges usually d ecreased with intensity, and activity at two or even three discrete latenci es was often observed in the same spike train. Latency shifts from one disc rete time range to another often occurred as intensity increased, Some shif ts could be attributed to responses to the opposite-polarity phase of the b iphasic pulse, In these cases, temporal dispersion and dynamic range were a pproximately equal for activity at each latency. A second type of latency s hift was also often observed, in which responses at each latency exhibited dissimilar temporal dispersion and dynamic range. This behavior was attribu ted to a centralward shift in the spike initiation site and it occurred for monophasic as well as biphasic signals. Several fibers exhibited dual late ncy activity with a 40-90 mu s time difference between response peaks. This may have stemmed from spike initiation at nodes on either side of the cell body. Increasing the Stimulus pulse rate to 800-1000 pps produced small in creases in temporal dispersion and proportionate increases in asymptotic di scharge rate and dynamic range, but thresholds did not improve and slopes o f rate-intensity functions (in spikes/s/dB) did not change. Responses to hi gh-rate stimuli also exhibited discrete latency increases when discharge ra tes exceeded 300-400 spikes/s, Spike by spike latencies in these cases depe nded strongly on the discharge history; Implications for high-rate speech p rocessing strategies are discussed. (C) 2000 Elsevier Science B.V. All righ ts reserved.