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Social reward is intact in BALB/c mice, attenuated by postnatal valproic acid treatment, and unaffected by GSTM1 knockout in a neurodevelopmental animal model of autism
Descriptive
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Text
TitleInfo
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Title
Social reward is intact in BALB/c mice, attenuated by postnatal valproic acid treatment, and unaffected by GSTM1 knockout in a neurodevelopmental animal model of autism
Identifier
ETD_650
Identifier
(type = hdl)
http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000056705
Language
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eng
Genre
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theses
Subject
(ID = SBJ-1);
(authority = RUETD)
Topic
Psychology
Subject
(ID = SBJ-2);
(authority = ETD-LCSH)
Topic
Autism--Etiology
Subject
(ID = SBJ-3);
(authority = ETD-LCSH)
Topic
Autism--Environmental aspects
Subject
(ID = SBJ-4);
(authority = ETD-LCSH)
Topic
Mice as laboratory animals
Subject
(ID = SBJ-5);
(authority = ETD-LCSH)
Topic
Reward (Psychology)
Abstract
(type = abstract)
In a neurodevelopmental model of autism with age, genetic background and toxicant exposure as factors, three experiments assessed social reward in adolescent mice using an adapted social conditioned bedding preference task. Autism is a neurodevelopmental disorder behaviorally defined by restricted and repetitive activities and interests, core impairments in communication, and pervasive deficits in social interaction. Although no single causal agent has been identified, a plausible candidate may be early toxicant exposure in individuals with genetic vulnerability. The generation of reactive oxygen species may be a mechanism shared by toxicants such as valproic acid, which leads to autistic-like symptoms in both mice and humans. Thus, these experiments examined the effects of BALB/c strain, GSTM1 mice lacking an enzyme involved in oxidative stress, and BALB/c mice treated with postnatal valproic acid, on social conditioning in adolescent mice. Results revealed intact social conditioning in BALB/c mice and GSTM1 mice. However, postnatal valproic acid treatment led to social conditioning deficits and perseverative responding in adolescent BALB/c mice. Collectively, these results corroborate previous studies suggesting that early postnatal toxicant exposure induces social deficits in adolescence. Use of the social conditioning paradigm allowed assessment of deficits in individual mice, reducing potential for experimental confounds during the test. Furthermore, these experiments lay the foundation for investigations of the effects of genotype-toxicant interaction on social conditioning or subsequent social behavior.
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electronic resource
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vi, 101 p. : ill.
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Ph.D.
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Includes bibliographical references
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Includes vita
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by Teresa Camille Parsons
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Parsons
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Teresa Camille
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1978-
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author
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Teresa Parsons
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Wagner
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George C
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chair
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George C Wagner
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Kusnecov
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Alexander
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internal member
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Advisory Committee
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Alexander Kusnecov
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(type = family)
Harris
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Sandra
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internal member
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Advisory Committee
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Sandra Harris
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Ming
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Xue
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outside member
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Advisory Committee
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Xue Ming
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Rutgers University
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degree grantor
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Graduate School - New Brunswick
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school
OriginInfo
DateCreated
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2010
DateOther
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2010-10
Place
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xx
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TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
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(type = host)
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Title
Graduate School - New Brunswick Electronic Theses and Dissertations
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rucore19991600001
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NjNbRU
Identifier
(type = doi)
doi:10.7282/T3NK3DS8
Genre
(authority = ExL-Esploro)
ETD doctoral
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Rights
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(ID = rulibRdec0006)
The author owns the copyright to this work.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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(type = personal)
Name
FamilyName
Parsons
GivenName
Teresa
Role
Copyright Holder
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Type
Permission or license
DateTime
2010-08-19 16:44:50
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Name
Teresa Parsons
Affiliation
Rutgers University. Graduate School - New Brunswick
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Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
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