Chemogenetic activation of cortical parvalbumin-positive interneurons reverses noise-induced impairments in gap detection

Samer Masri, Nakayla Chan, Tyler Marsh, Alexander Zinsmaier, David Schaub, Li Zhang, Weihua Wang, Shaowen Bao

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Exposure to loud noises not only leads to trauma and loss of output from the ear but also alters downstream central auditory circuits. A perceptual consequence of noise-induced central auditory disruption is impairment in gap-induced prepulse inhibition, also known as gap detection. Recent studies have implicated cortical parvalbumin (PV)-positive inhibitory interneurons in gap detection and prepulse inhibition. Here, we show that exposure to loud noises specifically reduces the density of cortical PV but not somatostatin (SOM)-positive interneurons in the primary auditory cortex in mice (C57BL/6) of both sexes. Optogenetic activation of PV neurons produced less cortical inhibition in noise-exposed than sham-exposed animals, indicative of reduced PV neuron function. Activation of SOM neurons resulted in similar levels of cortical inhibition in noise- and sham-exposed groups. Furthermore, chemogenetic activation of PV neurons with the hM3-based designer receptor exclusively activated by designer drugs completely reversed the impairments in gap detection for noise-exposed animals. These results support the notions that cortical PV neurons encode gap in sound and that PV neuron dysfunction contributes to noiseinduced impairment in gap detection.

Original languageEnglish (US)
Pages (from-to)8848-8857
Number of pages10
JournalJournal of Neuroscience
Volume41
Issue number42
DOIs
StatePublished - Oct 20 2021

Keywords

  • Auditory processing disorder
  • Gap detection
  • Hearing loss
  • Inhibition
  • Parvalbumin
  • Somatostatin

ASJC Scopus subject areas

  • General Neuroscience

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