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Effects on the fetal cholinergic basal forebrain following maternal immune activation
Descriptive
TitleInfo
Title
Effects on the fetal cholinergic basal forebrain following
maternal immune activation
maternal immune activation
Name
(type = personal)
NamePart
(type = family)
Pratt
NamePart
(type = given)
Lorelei
NamePart
(type = date)
1953-
DisplayForm
Lorelei Pratt
Role
RoleTerm
(authority = RULIB)
author
Name
(type = personal)
NamePart
(type = family)
Jonakait
NamePart
(type = given)
G Miller
DisplayForm
G Miller Jonakait
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
chair
Name
(type = personal)
NamePart
(type = family)
Morrell
NamePart
(type = given)
Joan I
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Joan I Morrell
Affiliation
Advisory Committee
Role
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(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Friedman
NamePart
(type = given)
Wilma
DisplayForm
Wilma Friedman
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Ponzio
NamePart
(type = given)
Nicholas M
DisplayForm
Nicholas M Ponzio
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
outside member
Name
(type = personal)
NamePart
(type = family)
DiCicco-Bloom
NamePart
(type = given)
Emanuel
DisplayForm
Emanuel DiCicco-Bloom
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
Graduate School - Newark
Role
RoleTerm
(authority = RULIB)
school
TypeOfResource
Text
Genre
(authority = marcgt)
theses
OriginInfo
DateCreated
(qualifier = exact)
2013
DateOther
(qualifier = exact);
(type = degree)
2013-01
CopyrightDate
(encoding = marc);
(point = start);
(qualifier = exact)
2013
Place
PlaceTerm
(type = code)
xx
Language
LanguageTerm
(authority = ISO639-2b);
(type = code)
eng
Abstract
(type = abstract)
Neurodevelopmental disorders such as autism and schizophrenia may result in part from maternal immune activation (MIA) during pregnancy. However, the mechanisms in the embryonic brain leading to these disorders in offspring remain unclear. Data suggest that interleukin-6 (IL-6) may be a key factor affecting fetal development following MIA. Abnormalities in the cholinergic basal forebrain (BF) are associated with neurodevelopmental disorders. Previous in vitro studies have shown that factors produced by activated microglia promote the cholinergic differentiation of precursors in the BF. It has not been demonstrated whether fetal microglia become activated in vivo following MIA or whether such activation results in increased numbers of BF cholinergic neurons. To test this, pregnant wild-type and IL-6 knock-out mice were injected with a viral mimic. Fetal/perinatal BFs of offspring were assayed for choline acetyltransferase (ChAT) activity and compared to offspring of saline-injected mice. The number of cholinergic neurons in BFs was quantified using stereological techniques. To determine fetal microglial activation status, lysates from enriched populations of microglial cells were analyzed for cytokine/chemokine protein production using LUMINEX® assays. Studies were performed in culture to determine whether certain elevated chemokines affect BF cholinergic development. Results show that following MIA, ChAT activity increases in the BF at embryonic days 16.5 (E16.5), E18.5 and postnatal day 1 (P1). Cholinergic cell number also increases. Fetal microglia produce higher levels of several cytokines and chemokines. Unexpectedly, ChAT activity is higher in control IL-6 KO BFs at E16.5 than in wild-types and MIA does not increase ChAT activity further. Non-microglial fetal brain cells also produce cytokines and chemokines. Non-microglial cells from control IL-6 KOs express increased levels of cytokines and chemokines compared to wild-types and MIA does not increase these levels. Culture studies suggest that a C-C chemokine receptor 5 (CCR5) ligand may be a factor affecting BF cell survival. These data reveal changes following MIA that could potentially affect neural development. The fetal microglial cytokine/chemokine profile is altered. Perinatal increases in ChAT activity may have long-lasting consequences. Results also suggest a role for IL-6 in regulating proper cytokine and chemokine balance during normal brain development.
Subject
(authority = RUETD)
Topic
Biology
RelatedItem
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TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
Identifier
ETD_4423
PhysicalDescription
Form
(authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
x, 158 p. : ill.
Note
(type = degree)
Ph.D.
Note
(type = bibliography)
Includes bibliographical references
Note
(type = vita)
Includes vita
Note
(type = statement of responsibility)
by Lorelei Pratt
Subject
(authority = ETD-LCSH)
Topic
Maternal-fetal exchange
Subject
(authority = ETD-LCSH)
Topic
Parasympathomimetic agents
Subject
(authority = ETD-LCSH)
Topic
Interleukin-6
Subject
(authority = ETD-LCSH)
Topic
Fetus--Development
Identifier
(type = hdl)
http://hdl.rutgers.edu/1782.1/rucore10002600001.ETD.000067622
RelatedItem
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TitleInfo
Title
Graduate School - Newark Electronic Theses and Dissertations
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rucore10002600001
Location
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(authority = marcorg);
(displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier
(type = doi)
doi:10.7282/T34Q7SQ5
Genre
(authority = ExL-Esploro)
ETD doctoral
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Rights
RightsDeclaration
(ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder
(type = personal)
Name
FamilyName
Pratt
GivenName
Lorelei
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime
(encoding = w3cdtf);
(qualifier = exact);
(point = start)
2012-12-15 15:30:31
AssociatedEntity
Name
Lorelei Pratt
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - Newark
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
RULTechMD
(ID = TECHNICAL1)
ContentModel
ETD
OperatingSystem
(VERSION = 5.1)
windows xp
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