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Klug, Achim; Khan, Asma; Burger, R. Michael; Bauer, Eric E.; Hurley, Laura M.; Yang, Lichuan; Grothe, Benedikt ORCID logoORCID: https://orcid.org/0000-0001-7317-0615; Halvorsen, Michele B. und Park, Thomas J. (2000): Latency as a function of intensity in auditory neurons: influences of central processing. In: Hearing Research, Bd. 148, Nr. 43497: S. 107-123

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Abstract

The response latencies of sensory neurons typically shorten with increases in stimulus intensity. In the central auditory system this phenomenon should have a significant impact on a number of auditory functions that depend critically on an integration of precisely timed neural inputs. Evidence from previous studies suggests that the auditory system not only copes with the potential problems associated with intensity-dependent latency change, but that it also modifies latency change to shape the response properties of many cells for specific functions. This observation suggests that intensity-dependent latency change may undergo functional transformations along the auditory neuraxis. The goal of our study was to explore these transformations by making a direct, quantitative comparison of intensity-dependent latency change among a number of auditory centers from the lower brainstem to the thalamus. We found two main ways in which intensity-dependent latency change transformed along the neuraxis: (1) the range of latency change increased substantially and (2) one particular type of latency change, which has been suggested to be associated with sensitivity to temporally segregated stimulus components, occurred only at the highest centers tested, the midbrain and thalamus. Additional testing in the midbrain (inferior colliculus) indicated that inhibitory inputs are involved in shaping latency change. Our findings demonstrate that the central auditory system modifies intensity-dependent latency changes. We suggest that these changes may be functionally incorporated, actively enhanced, or modified to suit specific functions of the auditory system. (C) 2000 Elsevier Science B.V. All rights reserved.

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