Humans are remarkably sensitive to brief interruptions of ongoing sound. Gap-detection thresholds (duration thresholds for detection of a brief silent gap in a noise or tone) are typically less than 6 ms in normal young adults, and often higher in older adults, patients with developmental disorders, or subjects with auditory processing difficulties. Gap-detection thresholds are therefore routinely measured in audiological clinics to assess the temporal acuity of auditory processing. However, despite the simplicity of the gap-in-noise detection task and its importance as a clinical tool, the neural mechanisms of gap detection are still poorly understood.

In this talk, I will discuss recent insights into the neural mechanisms of gap detection gained from combined neurophysiological and computational studies of an unusual mouse model of gap-detection deficits. As described in published work (Anderson and Linden 2016 J Neurosci 36:1977-95), we have discovered that neural responses to sound offsets (disappearances) play an important role in generating gap-in-noise sensitivity. In recent unpublished work, we have also found that adaptive gain control in the central auditory system serves to increase gap-in-noise sensitivity. Together, these results indicate that gap-in-noise detection relies not only on peripheral and brainstem mechanisms that produce precisely timed neural responses to sound onsets, but also on brainstem mechanisms that generate neural responses to sound offsets, and higher central auditory mechanisms of adaptation and intensity gain control. Elevated gap-detection thresholds in patients with auditory processing difficulties therefore could arise from several different auditory system abnormalities, which may be distinguishable with additional auditory tests.