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Opioid receptor like-1 receptor deficient mice show dysregulation of the hypothalamic pituitary adrenal axis following acute immunologic challenge with staphylococcal enterotoxin A
Descriptive
TypeOfResource
Text
TitleInfo
(ID = T-1)
Title
Opioid receptor like-1 receptor deficient mice show dysregulation of the hypothalamic pituitary adrenal axis following acute immunologic challenge with staphylococcal enterotoxin A
Identifier
ETD_2754
Identifier
(type = hdl)
http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000056573
Language
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(type = code)
eng
Genre
(authority = marcgt)
theses
Subject
(ID = SBJ-1);
(authority = RUETD)
Topic
Psychology
Subject
(ID = SBJ-2);
(authority = ETD-LCSH)
Topic
Opioids--Receptors
Subject
(ID = SBJ-3);
(authority = ETD-LCSH)
Topic
Immunology--Animal models
Subject
(ID = SBJ-4);
(authority = ETD-LCSH)
Topic
Stress (Physiology)--Endocrine aspect
Abstract
(type = abstract)
Opioid receptor like-1 receptor (ORL1) shares considerable sequence identity with the classical µ, δ, and κ opioid receptors yet shows no affinity to the classical opioid ligands. Rather, ORL1 is selective for its endogenous ligand, orphaninFQ/Nociceptin (OFQ/N). The nociceptin system is integral to many physiological processes (e.g., nociception) and plays a prominent role in regulation of the hypothalamic-pituitary-adrenal (HPA) axis, the stress response, and anxiety. Since immunologic stimuli exert stressor-like effects, the neuroendocrine and behavioral effects of the T-cell superantigen staphylococcal enterotoxin A (SEA) were tested in 129S6, ORL1 wildtype (ORL1+/+) and knockout (ORL1-/-) mice. Within 2 h of SEA challenge both genotypes showed elevated levels of plasma corticosterone, but only wildtypes remained elevated after 4 h. The effects of SEA on corticosterone levels were determined to be associated with changes in corticotropin releasing hormone (CRH), CRH receptor 1 (CRH-R1) and CRH-R2 mRNA expression in the hypothalamus. Moreover, SEA-induced changes in CRH and CRH-R1 were dependent on the presence of the ORL1 gene and suggest that activation of the ORL1 receptor may modulate positive and negative feedback control of CRH activity in the hypothalamus. These findings are consistent with the idea that ORL1 activation prolongs stress-induced levels of corticosterone, possibly through ORL1 dependent modulation of the CRH system. Furthermore, gustatory neophobia due to SEA challenge was augmented in ORL1-/- mice and is consistent with the anxiolytic role for the nociceptin system. In summary, these results suggest that the ORL1 gene may be necessary for normal HPA axis activity and may confer resistance to novelty-induced anorexia following acute SEA challenge in 129S6 mice.
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electronic resource
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ix, 85 p. : ill.
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application/pdf
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M.S.
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Includes bibliographical references
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by Elyse M Mallimo
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Mallimo
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Elyse M.
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1985-
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author
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Elyse Mallimo
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Kusnecov
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Alexander
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chair
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Advisory Committee
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Alexander Kusnecov
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Shors
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Tracey
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internal member
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Advisory Committee
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Tracey Shors
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Wagner
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George
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internal member
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Advisory Committee
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George Wagner
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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
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ETD
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TitleInfo
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/T33778GP
Genre
(authority = ExL-Esploro)
ETD graduate
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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
RightsHolder
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(type = personal)
Name
FamilyName
Mallimo
GivenName
Elyse
Role
Copyright Holder
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(ID = RE-1);
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Type
Permission or license
DateTime
2010-06-11 12:06:13
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(AUTHORITY = rulib)
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Copyright holder
Name
Elyse Mallimo
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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ETD
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application/pdf
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application/x-tar
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522240
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c46f2ba98534bb631e49f97ea7bf82dfaf66e5f9
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