Project Title

Gastrointestinal Alterations in Two Mouse Models That Are Associated With Social Behavior Deficits

Authors' Affiliations

Gracie Leamon, College of Public Health, East Tennessee State University, Johnson City, TN Michelle Chandley, Department of Biomedical Sciences, College of Public Health, ETSU Quillen College of Medicine, Johnson City, TN Evan Hunter Mason, MD Program, ETSU Quillen College of Medicine, Johnson City, TN Lindsey Stallworth, College of Clinical and Rehabilitative Health Sciences, East Tennessee State University, Johnson City, TN William A. Clark, College of Clinical and Rehabilitative Health Sciences, East Tennessee State University, Johnson City, TN

Location

Culp Room 217

Start Date

4-6-2022 9:30 AM

End Date

4-6-2022 9:45 AM

Faculty Sponsor’s Department

Biomedical Sciences

Name of Project's Faculty Sponsor

Michelle Chandley

Additional Sponsors

Scott Koterbay

Classification of First Author

Undergraduate Student

Competition Type

Non-Competitive

Type

Boland Symposium

Project's Category

Neuroscience

Abstract or Artist's Statement

The gastrointestinal (GI) tract is a diverse habitat for multiple microorganisms. Disturbances in the microbiome of the GI tract have been associated with psychiatric disorders including autism spectrum disorder (ASD). Individuals with ASD, when compared to neurotypical individuals, have demonstrated differing gut species. Also, it has been shown that microbial transplant therapies impact ASD symptoms in patients. Animal models of behaviors associated with ASD might offer insight into the actual role these microbial differences may occupy regarding symptoms. Unfortunately, ASD does not have an accepted animal model where the GI alterations have been thoroughly explored. In this study, we sought to determine if the microbiome and other GI alterations were observed in two potential mouse models of social behavior deficits, the genetic BTBR T+Itpr3tf/J (BTBR) mouse strain and an environmental mouse strain consisting of offspring of valproic acid (VA) treated pregnant controls. Both mouse models have been shown to exhibit social and repetitive behaviors that are found in human ASD. Using the Illumina MiSeq, we were able to identify taxonomy associated with 16S ribosomal DNA sequences extracted from fecal matter. We were able to compare the sequencing results from the two affected strains and a control C5BL/6J mouse strain for both female and male animals using the Qiagen CLC Genomics Workbench software. Overall, microbiome composition was found to be significantly different between the male control animals (N=13) when compared to the VA (N=14; p-value=.00003) or the BTBR (N=15; p-value=.0001) males using a PERMANOVA analysis. This was replicated in female groups where composition significantly differed between the control (N=14) and VA (N=14; p-value=.00003) or BTBR (N=14; p-value=.00001) females. Additionally, short-chain fatty acid analysis using gas capillary-based chromatography was used to examine acetate, butyrate, propionate, and valerate levels in feces. Only valerate levels were significantly lower (p

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Apr 6th, 9:30 AM Apr 6th, 9:45 AM

Gastrointestinal Alterations in Two Mouse Models That Are Associated With Social Behavior Deficits

Culp Room 217

The gastrointestinal (GI) tract is a diverse habitat for multiple microorganisms. Disturbances in the microbiome of the GI tract have been associated with psychiatric disorders including autism spectrum disorder (ASD). Individuals with ASD, when compared to neurotypical individuals, have demonstrated differing gut species. Also, it has been shown that microbial transplant therapies impact ASD symptoms in patients. Animal models of behaviors associated with ASD might offer insight into the actual role these microbial differences may occupy regarding symptoms. Unfortunately, ASD does not have an accepted animal model where the GI alterations have been thoroughly explored. In this study, we sought to determine if the microbiome and other GI alterations were observed in two potential mouse models of social behavior deficits, the genetic BTBR T+Itpr3tf/J (BTBR) mouse strain and an environmental mouse strain consisting of offspring of valproic acid (VA) treated pregnant controls. Both mouse models have been shown to exhibit social and repetitive behaviors that are found in human ASD. Using the Illumina MiSeq, we were able to identify taxonomy associated with 16S ribosomal DNA sequences extracted from fecal matter. We were able to compare the sequencing results from the two affected strains and a control C5BL/6J mouse strain for both female and male animals using the Qiagen CLC Genomics Workbench software. Overall, microbiome composition was found to be significantly different between the male control animals (N=13) when compared to the VA (N=14; p-value=.00003) or the BTBR (N=15; p-value=.0001) males using a PERMANOVA analysis. This was replicated in female groups where composition significantly differed between the control (N=14) and VA (N=14; p-value=.00003) or BTBR (N=14; p-value=.00001) females. Additionally, short-chain fatty acid analysis using gas capillary-based chromatography was used to examine acetate, butyrate, propionate, and valerate levels in feces. Only valerate levels were significantly lower (p