서브메뉴
검색
Neural Adaptation and Instability in the Mammalian Retina
Neural Adaptation and Instability in the Mammalian Retina
상세정보
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20260311091511.5
- ISBN
- 9798280780316
- DDC
- 571
- 저자명
- Khoussine, Jacob
- 서명/저자
- Neural Adaptation and Instability in the Mammalian Retina / Jacob Khoussine
- 발행사항
- [Sl] : The University of Wisconsin - Madison, 2025
- 형태사항
- 1 electronic resource (76 pages)
- 주기사항
- Source: Dissertations Abstracts International, Volume: 86-12, Section: B.
- 주기사항
- Advisors: Hoon, Mrinalini Committee members: Sinha, Raunak; Gamm, David; Felton, Elizabeth; Audhya, Anjon.
- 학위논문주기
- - Ph.D. : The University of Wisconsin - Madison, 2025.
- 초록/해제
- 요약Neural circuits can withstand moderate disruptions and still function, but there comes a threshold beyond which plasticity falters and networks collapse. This thesis investigates that boundary in the visual system using the mammalian retina as a model, revealing how neural circuits adapt to disruption and what occurs when their resilience is exceeded. Chapter 1 describes how light-driven activity and synaptic adjustments shape visual circuits early in life and how these adaptive processes preserve function in response to progressive input loss throughout life. Chapter 2 focuses on two mouse models of congenital stationary night blindness (CSNB) with either ~50% or 100% loss of ON pathway input. We used patch-clamp electrophysiology to record the intrinsic properties, synaptic inputs, and spike outputs of retinal ganglion cells, combined with single-cell immunohistochemistry to assess dendritic synapse composition, and contextualized these findings with assays of visual behavior in each model. Partial loss triggers structural adjustments that maintain signal output, whereas complete suppression overwhelms the circuit's capacity to adapt, leading to intrinsic changes and destabilizing bursts of aberrant activity. This contrast reveals a tipping point at which plasticity-driven alterations fail to preserve function. Chapter 3 examines how emerging retinal imaging methods and gene therapies might detect and correct such imbalances before they reach this critical threshold. Ultimately, the unifying theme of this thesis is that understanding visual neuroplasticity in health and disease is fundamental to preserving and restoring vision.
- 언어주기
- English
- 일반주제명
- Ophthalmology
- 일반주제명
- Neurosciences
- 일반주제명
- Cellular biology
- 키워드
- Neurophysiology
- 키워드
- Neuroplasticity
- 키워드
- Retina
- 기타저자
- The University of Wisconsin - Madison Cellular and Molecular Biology
- 기본자료저록
- Dissertations Abstracts International. 86-12B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
008260311s2025 us eng d■001000017358446
■00520260311091511.5
■006m o d
■007cr|nu||||||||
■020 ▼a9798280780316
■040 ▼aMiAaPQD▼beng▼cMiAaPQD▼erda
■082 ▼a571
■1001 ▼aKhoussine, Jacob▼eauthor.
■24510▼aNeural Adaptation and Instability in the Mammalian Retina ▼cJacob Khoussine
■260 ▼a[Sl]▼bThe University of Wisconsin - Madison▼c2025
■264 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2025
■300 ▼a1 electronic resource (76 pages)
■336 ▼atext▼btxt▼2rdacontent
■337 ▼acomputer▼bc▼2rdamedia
■338 ▼aonline resource▼bcr▼2rdacarrier
■500 ▼aSource: Dissertations Abstracts International, Volume: 86-12, Section: B.
■500 ▼aAdvisors: Hoon, Mrinalini Committee members: Sinha, Raunak; Gamm, David; Felton, Elizabeth; Audhya, Anjon.
■5021 ▼bPh.D.▼cThe University of Wisconsin - Madison▼d2025.
■520 ▼aNeural circuits can withstand moderate disruptions and still function, but there comes a threshold beyond which plasticity falters and networks collapse. This thesis investigates that boundary in the visual system using the mammalian retina as a model, revealing how neural circuits adapt to disruption and what occurs when their resilience is exceeded. Chapter 1 describes how light-driven activity and synaptic adjustments shape visual circuits early in life and how these adaptive processes preserve function in response to progressive input loss throughout life. Chapter 2 focuses on two mouse models of congenital stationary night blindness (CSNB) with either ~50% or 100% loss of ON pathway input. We used patch-clamp electrophysiology to record the intrinsic properties, synaptic inputs, and spike outputs of retinal ganglion cells, combined with single-cell immunohistochemistry to assess dendritic synapse composition, and contextualized these findings with assays of visual behavior in each model. Partial loss triggers structural adjustments that maintain signal output, whereas complete suppression overwhelms the circuit's capacity to adapt, leading to intrinsic changes and destabilizing bursts of aberrant activity. This contrast reveals a tipping point at which plasticity-driven alterations fail to preserve function. Chapter 3 examines how emerging retinal imaging methods and gene therapies might detect and correct such imbalances before they reach this critical threshold. Ultimately, the unifying theme of this thesis is that understanding visual neuroplasticity in health and disease is fundamental to preserving and restoring vision.
■546 ▼aEnglish
■590 ▼aSchool code: 0262
■650 4▼aOphthalmology
■650 4▼aNeurosciences
■650 4▼aCellular biology
■653 ▼aNeurophysiology
■653 ▼aNeuroplasticity
■653 ▼aRetina
■653 ▼aVisual processing
■653 ▼aElectrophysiology
■7102 ▼aThe University of Wisconsin - Madison▼bCellular and Molecular Biology.▼edegree granting institution.
■7201 ▼aHoon, Mrinalini▼edegree supervisor.
■7730 ▼tDissertations Abstracts International▼g86-12B.
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17358446▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
