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dc.contributor.authorMasri, S.
dc.contributor.authorChan, N.
dc.contributor.authorMarsh, T.
dc.contributor.authorZinsmaier, A.
dc.contributor.authorSchaub, D.
dc.contributor.authorZhang, L.
dc.contributor.authorWang, W.
dc.contributor.authorBao, S.
dc.date.accessioned2021-11-29T19:38:12Z
dc.date.available2021-11-29T19:38:12Z
dc.date.issued2021
dc.identifier.citationMasri, S., Chan, N., Marsh, T., Zinsmaier, A., Schaub, D., Zhang, L., Wang, W., & Bao, S. (2021). Chemogenetic activation of cortical parvalbumin-positive interneurons reverses noise-induced impairments in gap detection. Journal of Neuroscience.
dc.identifier.issn0270-6474
dc.identifier.pmid34452937
dc.identifier.doi10.1523/JNEUROSCI.2687-19.2021
dc.identifier.urihttp://hdl.handle.net/10150/662364
dc.description.abstractExposure 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. © 2021 the authors.
dc.language.isoen
dc.publisherSociety for Neuroscience
dc.rightsCopyright © 2021 the authors.
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.subjectAuditory processing disorder
dc.subjectGap detection
dc.subjectHearing loss
dc.subjectInhibition
dc.subjectParvalbumin
dc.subjectSomatostatin
dc.titleChemogenetic activation of cortical parvalbumin-positive interneurons reverses noise-induced impairments in gap detection
dc.typeArticle
dc.typetext
dc.contributor.departmentGraduate Program in Neuroscience, University of Arizona
dc.contributor.departmentDepartment of Physiology, University of Arizona
dc.contributor.departmentDepartment of Physiology, University of Arizona
dc.identifier.journalJournal of Neuroscience
dc.description.note6 month embargo; first published: 20 October 2021
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.
dc.eprint.versionFinal published version
dc.source.journaltitleJournal of Neuroscience


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