Auditory Temporal Acuity Probed With Cochlear Implant Stimulation and Cortical Recording

Authors:
  • JMJohn C. Middlebrooks
    John C. Middlebrooks
  • JYJustin D. Yao
    Justin D. Yao
  • PBPeter Bremen
    Peter Bremen
  • KHKenneth E. Hancock
    Kenneth E. Hancock
  • YCYoojin Chung
    Yoojin Chung
  • BDBertrand Delgutte
    Bertrand Delgutte
  • RBRalph E. Beitel
    Ralph E. Beitel
  • MVMaike Vollmer
    Maike Vollmer
  • MRMarcia W. Raggio
    Marcia W. Raggio
  • CSChristoph E. Schreiner
    Christoph E. Schreiner
Open Access
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Abstract
Cochlear implants stimulate the auditory nerve with amplitude-modulated (AM) electric pulse trains. Pulse rates >2,000 pulses per second (pps) have been hypothesized to enhance transmission of temporal information. Recent studies, however, have shown that higher pulse rates impair phase locking to sinusoidal AM in the auditory cortex and impair perceptual modulation detection. Here, we investigated the effects of high pulse rates on the temporal acuity of transmission of pulse trains to the auditory cortex. In anesthetized guinea pigs, signal-detection analysis was used to measure the thresholds for detection of gaps in pulse trains at rates of 254, 1,017, and 4,069 pps and in acoustic noise. Gap-detection thresholds decreased by an order of magnitude with increases in pulse rate from 254 to 4,069 pps. Such a pulse-rate dependence would likely influence speech reception through clinical speech processors. To elucidate the neural mechanisms of gap detection, we measured recovery from forward masking after a 196.6-ms pulse train. Recovery from masking was faster at higher carrier pulse rates and masking increased linearly with current level. We fit the data with a dual-exponential recovery function, consistent with a peripheral and a more central process. High-rate pulse trains evoked less central masking, possibly due to adaptation of the response in the auditory nerve. Neither gap detection nor forward masking varied with cortical depth, indicating that these processes are likely subcortical. These results indicate that gap detection and modulation detection are mediated by two separate neural mechanisms.

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