Synaptic inhibition shapes the temporal processing of sounds in auditory cortex, but the contribution of specific inhibitory cell types to temporal processing remains unclear. We recorded from parvalbumin-expressing (PV+) interneurons in auditory cortex to determine how they encode gaps in noise, a model of temporal processing more generally. We found that PV+ cells had stronger and more prevalent on-responses, off-responses, and postresponse suppression compared with presumed pyramidal cells. We summarize this pattern of differences as "deeper modulation" of gap responses in PV+ cells. Response latencies were also markedly faster for PV+ cells. We found a similar pattern of deeper modulation and faster latencies for responses to white noise bursts, suggesting that these are general properties of on- and off-responses in PV+ cells rather than specific features of gap encoding. These findings are consistent with a role for PV+ cells in providing dynamic gain control by pooling local activity. NEW & NOTEWORTHY We found that parvalbumin-expressing (PV+) interneurons in auditory cortex showed more deeply modulated responses to both gaps in noise and bursts of noise, suggesting that they are optimized for the rapid detection of stimulus transients.

Alzheimer's patients show auditory temporal processing deficits very early in disease progression, before the onset of major cognitive impairments. In addition to potentially contributing to speech perception and communication deficits in patients, this also represents a potential early biomarker for Alzheimer's. For this reason, tests of temporal processing such as gap detection have been proposed as an early diagnosis tool. For a biomarker such as gap detection deficits to have maximum clinical value, it is important to understand what underlying neuropathology it reflects. For example, temporal processing deficits could arise from alterations at cortical, midbrain, or brainstem levels. Mouse models of Alzheimer's disease can provide the ability to reveal in detail the molecular and circuit pathology underlying disease symptoms. Here we tested whether 5XFAD mice, a leading Alzheimer's mouse model, exhibit impaired temporal processing. We found that 5XFAD mice showed robust gap detection deficits. Gap detection deficits were first detectable at about 2 months of age and became progressively worse, especially for males and for longer gap durations. We conclude that 5XFAD mice are well-suited to serve as a model for understanding the circuit mechanisms that contribute to Alzheimer's-related gap detection deficits.