東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Roles of Parvalbumin-Expressing Inte...

Masri, Samer.

FindBook

Google Book

Amazon

博客來

Roles of Parvalbumin-Expressing Interneurons in Physiological Changes to Primary Auditory Cortex After Hearing Loss and Blast Exposure.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Roles of Parvalbumin-Expressing Interneurons in Physiological Changes to Primary Auditory Cortex After Hearing Loss and Blast Exposure./
作者:	Masri, Samer.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2020,
面頁冊數:	124 p.
附註:	Source: Dissertations Abstracts International, Volume: 82-02, Section: B.
Contained By:	Dissertations Abstracts International82-02B.
標題:	Nanoscience. -
電子資源:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28002884
ISBN:	9798662484856

Roles of Parvalbumin-Expressing Interneurons in Physiological Changes to Primary Auditory Cortex After Hearing Loss and Blast Exposure.
Masri, Samer.

Roles of Parvalbumin-Expressing Interneurons in Physiological Changes to Primary Auditory Cortex After Hearing Loss and Blast Exposure. - Ann Arbor : ProQuest Dissertations & Theses, 2020 - 124 p.

Source: Dissertations Abstracts International, Volume: 82-02, Section: B.

Thesis (Ph.D.)--The University of Arizona, 2020.

This item must not be sold to any third party vendors.

Hearing loss affects approximately 1 in 8 Americans and has a significant impact on quality of life, often leading to tinnitus and central auditory processing disorder. Hearing loss causes a cascade of changes to the auditory processing pathway, starting with death of hair cells in the inner ear and ultimately causing a series of physiological changes in primary auditory cortex (AI). Blast exposure commonly affects veterans and can lead to hearing loss as well as Traumatic Brain Injury (TBI), which damages the soft tissue and vasculature of the central nervous system and can independently cause central auditory processing disorder. The distinct effects of hearing loss and TBI on auditory processing remain poorly understood. Further research is needed to identify the role of AI in auditory processing deficits after hearing loss and/or TBI, as well as to identify specific cellular mechanisms to serve as targets for potential therapeutic approaches. First, I identify changes to the primary auditory cortex of rats following blast exposure with associated hearing loss. This includes distortions in the normal tonotopic frequency map in the form of random, frequency specific expansions. Additionally, there are associated changes to the hearing threshold and bandwidth of frequency tuning at individual cortical recording sites. These changes outline broad physiological deficits in auditory processing in primary auditory cortex after blast exposure.Next, I show that blast exposure alone can impair temporal processing in AI, but concurrent hearing loss dramatically exacerbates these impairments. I dissociate the effects of blast exposure and hearing loss by protecting either one or both ears from hearing loss during blast exposure. While blast exposure without hearing loss causes deficits in temporal processing which could lead to central auditory processing disorder, blast exposure with associated hearing loss causes more numerous and severe deficits. Specifically, only blast exposure with concurrent hearing loss reduces the expression of the Parvalbumin protein in AI and causes deficits in gap detection behavior, which is used as a test for potential tinnitus.Finally, I show that hearing loss alone causes a set of changes to Parvalbumin-expressing inhibitory interneurons (PV neurons) in AI. This includes a reduction of Parvalbumin expression in AI, changes to the gene expression profiles of PV neurons, and an overall reduction in the inhibitory output of PV neurons. These changes are not mirrored in another population of neurons called Somatostatin-expressing interneurons. I show that deficits in gap detection behavior following hearing loss can be rescued by Chemogenetic activation of PV neurons in AI.

ISBN: 9798662484856Subjects--Topical Terms:

587832
Nanoscience.
Subjects--Index Terms:

Auditory

Roles of Parvalbumin-Expressing Interneurons in Physiological Changes to Primary Auditory Cortex After Hearing Loss and Blast Exposure.
LDR:03966nmm a2200373 4500 001 2279717
005 20210823083426.5
008 220723s2020 ||||||||||||||||| ||eng d
020 $a 9798662484856
035 $a (MiAaPQ)AAI28002884
035 $a AAI28002884
040 $a MiAaPQ $c MiAaPQ
100 1 $a Masri, Samer. $3 3558191
245 1 0 $a Roles of Parvalbumin-Expressing Interneurons in Physiological Changes to Primary Auditory Cortex After Hearing Loss and Blast Exposure.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2020
300 $a 124 p.
500 $a Source: Dissertations Abstracts International, Volume: 82-02, Section: B.
500 $a Advisor: Bao, Shaowen;Fuglevand, Andrew.
502 $a Thesis (Ph.D.)--The University of Arizona, 2020.
506 $a This item must not be sold to any third party vendors.
520 $a Hearing loss affects approximately 1 in 8 Americans and has a significant impact on quality of life, often leading to tinnitus and central auditory processing disorder. Hearing loss causes a cascade of changes to the auditory processing pathway, starting with death of hair cells in the inner ear and ultimately causing a series of physiological changes in primary auditory cortex (AI). Blast exposure commonly affects veterans and can lead to hearing loss as well as Traumatic Brain Injury (TBI), which damages the soft tissue and vasculature of the central nervous system and can independently cause central auditory processing disorder. The distinct effects of hearing loss and TBI on auditory processing remain poorly understood. Further research is needed to identify the role of AI in auditory processing deficits after hearing loss and/or TBI, as well as to identify specific cellular mechanisms to serve as targets for potential therapeutic approaches. First, I identify changes to the primary auditory cortex of rats following blast exposure with associated hearing loss. This includes distortions in the normal tonotopic frequency map in the form of random, frequency specific expansions. Additionally, there are associated changes to the hearing threshold and bandwidth of frequency tuning at individual cortical recording sites. These changes outline broad physiological deficits in auditory processing in primary auditory cortex after blast exposure.Next, I show that blast exposure alone can impair temporal processing in AI, but concurrent hearing loss dramatically exacerbates these impairments. I dissociate the effects of blast exposure and hearing loss by protecting either one or both ears from hearing loss during blast exposure. While blast exposure without hearing loss causes deficits in temporal processing which could lead to central auditory processing disorder, blast exposure with associated hearing loss causes more numerous and severe deficits. Specifically, only blast exposure with concurrent hearing loss reduces the expression of the Parvalbumin protein in AI and causes deficits in gap detection behavior, which is used as a test for potential tinnitus.Finally, I show that hearing loss alone causes a set of changes to Parvalbumin-expressing inhibitory interneurons (PV neurons) in AI. This includes a reduction of Parvalbumin expression in AI, changes to the gene expression profiles of PV neurons, and an overall reduction in the inhibitory output of PV neurons. These changes are not mirrored in another population of neurons called Somatostatin-expressing interneurons. I show that deficits in gap detection behavior following hearing loss can be rescued by Chemogenetic activation of PV neurons in AI.
590 $a School code: 0009.
650 4 $a Nanoscience. $3 587832
650 4 $a Physiology. $3 518431
653 $a Auditory
653 $a Blast
653 $a Cortex
653 $a Hearing loss
653 $a Interneuron
653 $a Parvalbumin
690 $a 0565
690 $a 0719
710 2 $a The University of Arizona. $b Neuroscience. $3 1267736
773 0 $t Dissertations Abstracts International $g 82-02B.
790 $a 0009
791 $a Ph.D.
792 $a 2020
793 $a English
856 4 0 $u https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28002884