語系:
繁體中文
English
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
Regulation of Memory by the Actin-Bi...
~
Merovitch, Neil Henry.
FindBook
Google Book
Amazon
博客來
Regulation of Memory by the Actin-Binding Protein Cofilin.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Regulation of Memory by the Actin-Binding Protein Cofilin./
作者:
Merovitch, Neil Henry.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2023,
面頁冊數:
211 p.
附註:
Source: Dissertations Abstracts International, Volume: 85-01, Section: B.
Contained By:
Dissertations Abstracts International85-01B.
標題:
Neurosciences. -
電子資源:
https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30418715
ISBN:
9798379763800
Regulation of Memory by the Actin-Binding Protein Cofilin.
Merovitch, Neil Henry.
Regulation of Memory by the Actin-Binding Protein Cofilin.
- Ann Arbor : ProQuest Dissertations & Theses, 2023 - 211 p.
Source: Dissertations Abstracts International, Volume: 85-01, Section: B.
Thesis (Ph.D.)--University of Toronto (Canada), 2023.
The concept of disability is complex, constantly evolving and hard for many to understand. Disabilities, including those that are non-apparent such as some neurodevelopmental disorders, are often associated with negative preconceptions. Though neurodevelopmental disorders can affect language, speech, learning, memory, motor skills and other functions, individuals with these disorders can still lead meaningful lives. While many developmental disorders are associated with impaired learning and memory, different stages and types of memory can be affected. These impairments are often correlated with altered neuronal structure or function. Therefore, understanding the molecular mechanisms is important to better understand neurodevelopmental disorders. One process that is important for neuronal development is remodeling of the actin cytoskeleton. This remodeling is regulated by the actin binding protein cofilin, but its role in learning and memory remains unclear. Physiologically relevant manipulations of cofilin activity in vivo provide new opportunities for examining its function in learning and memory. Therefore, in this thesis, I examined three objectives to determine how cofilin overexpression in vivo affects the actin cytoskeleton and memory. I first characterized two novel transgenic mouse models that allow for either overexpression of wild-type or constitutively inactive forms of cofilin with spatial and temporal regulation. Expression of transgenic cofilin was robustly localized in excitatory neurons and processes in both mouse models. However, rod-like structures thought to be cofilin-actin aggregates were observed in cofilin overexpressing mice. I then showed that cofilin overexpression impaired short-term social novelty recognition, which was rescued by reversible transgene expression. Though it is unclear if the impairment was due to an underlying deficit in recognizing novelty. In contrast, some mice expressing constitutively inactive cofilin exhibited a possible immobility phenotype. However, further testing is required to determine the reproducibility of these impairments. Finally, cofilin-overexpressing zebrafish showed transgene expression throughout the nervous system, with rod-like structures in neuronal processes similar to those in mice with no effect on locomotion. Together, these results suggest that the novel transgenic cofilin models provide valuable tools for future research on the roles of cofilin and actin regulation in a variety of neuronal processes.
ISBN: 9798379763800Subjects--Topical Terms:
588700
Neurosciences.
Subjects--Index Terms:
Actin
Regulation of Memory by the Actin-Binding Protein Cofilin.
LDR
:03699nmm a2200409 4500
001
2401053
005
20241015112508.5
006
m o d
007
cr#unu||||||||
008
251215s2023 ||||||||||||||||| ||eng d
020
$a
9798379763800
035
$a
(MiAaPQ)AAI30418715
035
$a
AAI30418715
035
$a
2401053
040
$a
MiAaPQ
$c
MiAaPQ
100
1
$a
Merovitch, Neil Henry.
$0
(orcid)0000-0002-0107-8454
$3
3771114
245
1 0
$a
Regulation of Memory by the Actin-Binding Protein Cofilin.
260
1
$a
Ann Arbor :
$b
ProQuest Dissertations & Theses,
$c
2023
300
$a
211 p.
500
$a
Source: Dissertations Abstracts International, Volume: 85-01, Section: B.
500
$a
Advisor: Lefebvre, Julie;Jia, Zhengping.
502
$a
Thesis (Ph.D.)--University of Toronto (Canada), 2023.
520
$a
The concept of disability is complex, constantly evolving and hard for many to understand. Disabilities, including those that are non-apparent such as some neurodevelopmental disorders, are often associated with negative preconceptions. Though neurodevelopmental disorders can affect language, speech, learning, memory, motor skills and other functions, individuals with these disorders can still lead meaningful lives. While many developmental disorders are associated with impaired learning and memory, different stages and types of memory can be affected. These impairments are often correlated with altered neuronal structure or function. Therefore, understanding the molecular mechanisms is important to better understand neurodevelopmental disorders. One process that is important for neuronal development is remodeling of the actin cytoskeleton. This remodeling is regulated by the actin binding protein cofilin, but its role in learning and memory remains unclear. Physiologically relevant manipulations of cofilin activity in vivo provide new opportunities for examining its function in learning and memory. Therefore, in this thesis, I examined three objectives to determine how cofilin overexpression in vivo affects the actin cytoskeleton and memory. I first characterized two novel transgenic mouse models that allow for either overexpression of wild-type or constitutively inactive forms of cofilin with spatial and temporal regulation. Expression of transgenic cofilin was robustly localized in excitatory neurons and processes in both mouse models. However, rod-like structures thought to be cofilin-actin aggregates were observed in cofilin overexpressing mice. I then showed that cofilin overexpression impaired short-term social novelty recognition, which was rescued by reversible transgene expression. Though it is unclear if the impairment was due to an underlying deficit in recognizing novelty. In contrast, some mice expressing constitutively inactive cofilin exhibited a possible immobility phenotype. However, further testing is required to determine the reproducibility of these impairments. Finally, cofilin-overexpressing zebrafish showed transgene expression throughout the nervous system, with rod-like structures in neuronal processes similar to those in mice with no effect on locomotion. Together, these results suggest that the novel transgenic cofilin models provide valuable tools for future research on the roles of cofilin and actin regulation in a variety of neuronal processes.
590
$a
School code: 0779.
650
4
$a
Neurosciences.
$3
588700
650
4
$a
Physiology.
$3
518431
650
4
$a
Behavioral sciences.
$3
529833
653
$a
Actin
653
$a
ADF
653
$a
Cofilin
653
$a
Zebrafish
653
$a
Neurodevelopmental disorders
653
$a
Impairments
690
$a
0317
690
$a
0719
690
$a
0602
710
2
$a
University of Toronto (Canada).
$b
Physiology.
$3
3285885
773
0
$t
Dissertations Abstracts International
$g
85-01B.
790
$a
0779
791
$a
Ph.D.
792
$a
2023
793
$a
English
856
4 0
$u
https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30418715
筆 0 讀者評論
館藏地:
全部
電子資源
出版年:
卷號:
館藏
1 筆 • 頁數 1 •
1
條碼號
典藏地名稱
館藏流通類別
資料類型
索書號
使用類型
借閱狀態
預約狀態
備註欄
附件
W9509373
電子資源
11.線上閱覽_V
電子書
EB
一般使用(Normal)
在架
0
1 筆 • 頁數 1 •
1
多媒體
評論
新增評論
分享你的心得
Export
取書館
處理中
...
變更密碼
登入