title: Perceptual gap detection is mediated by gap termination responses in auditory cortex.
abstract: BACKGROUND
  Understanding speech in the presence of background noise often becomes increasingly difficult with age. These age-related speech processing deficits reflect impairments in temporal acuity. Gap detection is a model for temporal acuity in speech processing in which a gap inserted in white noise acts as a cue that attenuates subsequent startle responses. Lesion studies have shown that auditory cortex is necessary for the detection of brief gaps, and auditory cortical neurons respond to the end of the gap with a characteristic burst of spikes called the gap termination response (GTR). However, it remains unknown whether and how the GTR plays a causal role in gap detection. We tested this by optogenetically suppressing the activity of somatostatin- or parvalbumin-expressing inhibitory interneurons, or CaMKII-expressing excitatory neurons, in auditory cortex of behaving mice during specific epochs of a gap detection protocol.
  
  
  RESULTS
  Suppressing interneuron activity during the postgap interval enhanced gap detection. Suppressing excitatory cells during this interval attenuated gap detection. Suppressing activity preceding the gap had the opposite behavioral effects, whereas prolonged suppression across both intervals had no effect on gap detection.
  
  
  CONCLUSIONS
  In addition to confirming cortical involvement, we demonstrate here for the first time a causal relationship between postgap neural activity and perceptual gap detection. Furthermore, our results suggest that gap detection involves an ongoing comparison of pre- and postgap spiking activity. Finally, we propose a simple yet biologically plausible neural circuit that reproduces each of these neural and behavioral results.
authors: Institute of Neuroscience, University of Oregon, Eugene, OR 97405, USA.
authors: Aldis P
authors: AP
authors: Weible
authors: Institute of Neuroscience, University of Oregon, Eugene, OR 97405, USA.
authors: Alexandra K
authors: AK
authors: Moore
authors: Institute of Neuroscience, University of Oregon, Eugene, OR 97405, USA.
authors: Christine
authors: C
authors: Liu
authors: Institute of Neuroscience, University of Oregon, Eugene, OR 97405, USA.
authors: Leah
authors: L
authors: DeBlander
authors: Institute of Neuroscience, University of Oregon, Eugene, OR 97405, USA.
authors: Haiyan
authors: H
authors: Wu
authors: Institute of Neuroscience, University of Oregon, Eugene, OR 97405, USA; Kavli Institute, 7491 Trondheim, Norway.
authors: Clifford
authors: C
authors: Kentros
authors: Institute of Neuroscience, University of Oregon, Eugene, OR 97405, USA. Electronic address: wehr@uoregon.edu.
authors: Michael
authors: M
authors: Wehr
mesh_terms: D000161:Acoustic Stimulation; D000704:Analysis of Variance; D000818:Animals; D001303:Auditory Cortex / Q000502:physiology*; D001307:Auditory Perception / Q000502:physiology*; D007395:Interneurons / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D008959:Models, Neurological; D062308:Optogenetics; D010320:Parvalbumins / Q000378:metabolism; D013004:Somatostatin / Q000378:metabolism; D013997:Time Factors
chemical_list: D010320:Parvalbumins; D013004:Somatostatin