자료유형  

 학위논문

Control Number  

0016934483

International Standard Book Number  

9798380469531

Dewey Decimal Classification Number  

658

Main Entry-Personal Name  

Robinson, Beatriz Gwendolyn.

Publication, Distribution, etc. (Imprint  

[S.l.] : Stanford University., 2023

Publication, Distribution, etc. (Imprint  

Ann Arbor : ProQuest Dissertations & Theses, 2023

Physical Description  

1 online resource(98 p.)

General Note  

Source: Dissertations Abstracts International, Volume: 85-04, Section: A.

General Note  

Advisor: Kaltschmidt, Julia.

Dissertation Note  

Thesis (Ph.D.)--Stanford University, 2023.

Restrictions on Access Note  

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

Summary, Etc.  

요약Autism spectrum disorder (ASD) is a neurodevelopmental disorder that is characterized by deficits in social behavior, communication, and repetitive behaviors. Along with these hallmarks, gastrointestinal symptoms impact a significant portion of individuals with ASD, however, the reason underlying this association is not well understood. In Chapter 1of this dissertation, I provide a brief introduction to ASD and background information on what is known about the gastrointestinal tract and sensory dysfunction in ASD. Additionally, I provide background information on the enteric nervous system (ENS), which regulates gastrointestinal function, and review what is known about ASDrelated gene function in the ENS.In Chapter 2, I describe original research on the role of ASD-related cell adhesion molecule, Caspr2, in gastrointestinal function and the ENS. I characterize Caspr2's expression pattern in both the small intestine and colon and find that it is predominantly expressed in enteric sensory neurons. Notably, its expression is nearly exclusive to sensory neurons in the colon, which is in line with its expression pattern in sensory neurons of the PNS and CNS. I then explore the functional role of Caspr2 using the ASD mouse model, Caspr2-/- and find accelerated colonic function in the Caspr2knockout. The findings suggest that Caspr2 may play a role in sensory function of the ENS and that in its absence, GI motility is altered. Taken together, these findings suggest that further investigation into the sensory neurons of the ENS may give insight into ASD-related GI dysfunction.In Chapter 3, I provide an overview of the findings presented and provide additional discussion on future directions for this research.

Subject Added Entry-Topical Term  

Comorbidity.

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Behavior.

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Anxiety.

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Food.

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Brain research.

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Mutation.

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Neurosciences.

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Esophagus.

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Constipation.

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Stomach.

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Small intestine.

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Smooth muscle.

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Neurons.

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Cell adhesion & migration.

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Permeability.

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Colon.

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Sensory perception.

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Autism.

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Nervous system.

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Spinal cord.

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Enzymes.

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Morphology.

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Motility.

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Cellular biology.

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Clinical psychology.

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Disability studies.

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Psychology.

Added Entry-Corporate Name  

Stanford University.

Host Item Entry  

Dissertations Abstracts International. 85-04A.

Host Item Entry  

Dissertation Abstract International

Electronic Location and Access  

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Control Number  

joongbu:642160