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ERE-independent ERα signalling in feeding and exploratory behaviors

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TitleInfo
Title
ERE-independent ERα signalling in feeding and exploratory behaviors
Name (type = personal)
NamePart (type = family)
Yasrebi
NamePart (type = given)
Ali
NamePart (type = date)
1987-
DisplayForm
Ali Yasrebi
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Roepke
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Troy A
DisplayForm
Troy A Roepke
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
Name (type = personal)
NamePart (type = family)
Bello
NamePart (type = given)
Nicholas T
DisplayForm
Nicholas T Bello
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Bagnell
NamePart (type = given)
Carol A
DisplayForm
Carol A Bagnell
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Samuels
NamePart (type = given)
Benjamin A
DisplayForm
Benjamin A Samuels
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
outside member
Name (type = corporate)
NamePart
Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
Name (type = corporate)
NamePart
School of Graduate Studies
Role
RoleTerm (authority = RULIB)
school
TypeOfResource
Text
Genre (authority = marcgt)
theses
OriginInfo
DateCreated (encoding = w3cdtf); (keyDate = yes); (qualifier = exact)
2019
DateOther (encoding = w3cdtf); (qualifier = exact); (type = degree)
2019-10
CopyrightDate (encoding = w3cdtf); (qualifier = exact)
2019
Language
LanguageTerm (authority = ISO 639-3:2007); (type = text)
English
Abstract (type = abstract)
The reproductive steroid hormone, 17β-estradiol (E2), controls feeding and exploratory behaviors associated with mood disorders. The loss of circulating E2 puts menopausal women at an increased risk for developing obesity and mood disorders when compared to premenopausal women. Therefore, it is critically important to understand the role of sex steroids and their receptors in the neuroendocrine control of feeding and mood. The goal of this project is to understand the role of estrogen response Element (ERE)-dependent and ERE-independent ERα signaling on behavior by characterizing feeding patters and exploratory behaviors in male and female mice lacking either total ERα signaling or lacking ERE-dependent ERα signaling. We hypothesize that ERE-independent ERα is partially sufficient to restore feeding and exploratory behaviors that are lost in total ERα knockout mice. We tested three strains of mice: two ERα transgenic models, a total ERα knock out (ERKO) and a novel ERα knock in/knock out (KIKO) that lacks a functional DNA-binding domain) and their wild type (WT) C57 littermates using a real-time feeding behavior monitoring system and series of standard behavior tests (open field tests, elevated plus maze, forced swim test). To test our hypothesis FI and meal patterns were observed while the animals were given ad libitum access to a LFD (Experiment 1a) followed by HFD (Experiment 1b). A separate set of animals the response to fasting was monitored for 24 h after caloric restriction (Experiment 1c). Exploratory, depressive, and locomotor behavior testing was conducted on mice from Experiments 1a/b (open field, elevated plus maze, forced swim test). Each experiment was initially done with intact animals and then again repeated in ovariectomized (OVX) animals split into either an oil treated control group or an E2-treated group. We observed ERE-dependent mechanisms are the main modulator of homeostatic LFD feeding meal patterns while ERE- independent ERα signaling was involved in the control of palatable, high-fat diet food intake. During refeeding, ERE-independent mechanisms contribute to a decreased first meal food intake and slower rate of ingestion. When observed during a series of behavior tests, WT animals explored more, regardless of treatment (differences could be attributed to higher levels of locomotor activity in WT). However, similarities between WT and KIKO females in the EPM indicate that ERE-independent pathways may contribute towards reducing anxiety measures, independent of locomotor activity. WT females were shown to have a decreased free float time, indicating ERE dependent signaling may be influencing despair like tendencies. Collectively, these suggest that both ERE-dependent and -independent ERαsignaling are involved with both feeding and anxiety like homeostatic parameters.
Subject (authority = RUETD)
Topic
Endocrinology and Animal Biosciences
Subject (authority = local)
Topic
Estrogen receptor alpha
Subject (authority = LCSH)
Topic
Estrogen -- Receptors
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_10175
PhysicalDescription
Form (authority = gmd)
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
1 online resource (xi, 134 pages) : illustrations
Note (type = degree)
M.S.
Note (type = bibliography)
Includes bibliographical references
RelatedItem (type = host)
TitleInfo
Title
School of Graduate Studies Electronic Theses and Dissertations
Identifier (type = local)
rucore10001600001
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier (type = doi)
doi:10.7282/t3-kykn-9894
Genre (authority = ExL-Esploro)
ETD graduate
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Rights

RightsDeclaration (ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Yasrebi
GivenName
Ali
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2019-08-20 08:56:38
AssociatedEntity
Name
Ali Yasrebi
Role
Copyright holder
Affiliation
Rutgers University. School of Graduate Studies
AssociatedObject
Type
License
Name
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.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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Technical

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ETD
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windows xp
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1.4
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DateCreated (point = end); (encoding = w3cdtf); (qualifier = exact)
2019-08-20T16:02:57
DateCreated (point = end); (encoding = w3cdtf); (qualifier = exact)
2019-08-20T16:02:57
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