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Nervous System Function and Behavior in C. elegans Embryos
Nervous System Function and Behavior in C. elegans Embryos
상세정보
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20260202105134
- ISBN
- 9798265409959
- DDC
- 574
- 서명/저자
- Nervous System Function and Behavior in C. elegans Embryos
- 발행사항
- [Sl] : Harvard University, 2025
- 발행사항
- Ann Arbor : ProQuest Dissertations & Theses, 2025
- 형태사항
- 180 p
- 주기사항
- Source: Dissertations Abstracts International, Volume: 87-05, Section: B.
- 주기사항
- Advisor: Kaplan, Joshua M.
- 학위논문주기
- Thesis (Ph.D.)--Harvard University, 2025.
- 초록/해제
- 요약Events in early brain development are known to have profound impacts on later-life developmental outcomes. Most studies of circuit function and behavior use post- natal samples, likely due to the inaccessibility of intact embryos. How does nervous system function emerge and begin to control behavior during embryonic development? The optically accessible C. elegans embryo provides a powerful tool with which to address this question. GABA signaling is proposed to play important roles in circuit formation and plasticity, making GABA an interesting molecule to study in the context of embryonic nervous system function. We find that GABA release from developing motor neurons occurs prior to localization of pre- and post-synaptic ion channels in the nerve ring. Synaptic vesicle release contributes to but is not required for early motor neuron GABA release. Although bestrophin channels are known to mediate non-synaptic GABA release from glia, we find that bestrophins act in neurons to promote synaptic GABA release. These results indicate a role for non-synaptic GABA transmission in prenatal circuits. Previous work described a sleep-like behavior in late embryonic development. We took two approaches to identify developmental and circuit mechanisms underlying late embryonic behavior. First, we screened genes associated with autism spectrum disorder (ASD), which is theorized to have roots in early neurodevelopment. Several ASD risk genes regulate embryonic sleep-like behavior. An allele of CaV1 (with an equivalent amino acid change to a Timothy Syndrome allele) alters embryonic behavior by its effects downstream of the sleep active neuron RIS. Additionally, genes required for sensory neuron function are required for wild type behavior, suggesting sensory neurons regulate circuit function before the presence of externally generated sensory cues. These results define elements underlying embryonic neural circuit function.
- 일반주제명
- Biology
- 일반주제명
- Neurosciences
- 일반주제명
- Developmental biology
- 일반주제명
- Cellular biology
- 키워드
- Genetics
- 키워드
- Synapse
- 기타저자
- Harvard University Biological and Biomedical Sciences
- 기본자료저록
- Dissertations Abstracts International. 87-05B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
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■006m o d
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■020 ▼a9798265409959
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■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a574
■1001 ▼aMarvel-Coen, James.
■24510▼aNervous System Function and Behavior in C. elegans Embryos
■260 ▼a[Sl]▼bHarvard University▼c2025
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2025
■300 ▼a180 p
■500 ▼aSource: Dissertations Abstracts International, Volume: 87-05, Section: B.
■500 ▼aAdvisor: Kaplan, Joshua M.
■5021 ▼aThesis (Ph.D.)--Harvard University, 2025.
■520 ▼aEvents in early brain development are known to have profound impacts on later-life developmental outcomes. Most studies of circuit function and behavior use post- natal samples, likely due to the inaccessibility of intact embryos. How does nervous system function emerge and begin to control behavior during embryonic development? The optically accessible C. elegans embryo provides a powerful tool with which to address this question. GABA signaling is proposed to play important roles in circuit formation and plasticity, making GABA an interesting molecule to study in the context of embryonic nervous system function. We find that GABA release from developing motor neurons occurs prior to localization of pre- and post-synaptic ion channels in the nerve ring. Synaptic vesicle release contributes to but is not required for early motor neuron GABA release. Although bestrophin channels are known to mediate non-synaptic GABA release from glia, we find that bestrophins act in neurons to promote synaptic GABA release. These results indicate a role for non-synaptic GABA transmission in prenatal circuits. Previous work described a sleep-like behavior in late embryonic development. We took two approaches to identify developmental and circuit mechanisms underlying late embryonic behavior. First, we screened genes associated with autism spectrum disorder (ASD), which is theorized to have roots in early neurodevelopment. Several ASD risk genes regulate embryonic sleep-like behavior. An allele of CaV1 (with an equivalent amino acid change to a Timothy Syndrome allele) alters embryonic behavior by its effects downstream of the sleep active neuron RIS. Additionally, genes required for sensory neuron function are required for wild type behavior, suggesting sensory neurons regulate circuit function before the presence of externally generated sensory cues. These results define elements underlying embryonic neural circuit function.
■590 ▼aSchool code: 0084.
■650 4▼aBiology
■650 4▼aNeurosciences
■650 4▼aDevelopmental biology
■650 4▼aCellular biology
■653 ▼aCaenorhabditis elegans
■653 ▼aEmbryonic development
■653 ▼aGenetics
■653 ▼aSynapse
■690 ▼a0306
■690 ▼a0317
■690 ▼a0758
■690 ▼a0379
■71020▼aHarvard University▼bBiological and Biomedical Sciences.
■7730 ▼tDissertations Abstracts International▼g87-05B.
■790 ▼a0084
■791 ▼aPh.D.
■792 ▼a2025
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17359539▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
