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The Neuropeptide VGF is Reduced in Human Bipolar Postmortem Brain and Contributes to Some of the Behavioral and Molecular Effects of Lithium

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Text
TitleInfo
Title
The Neuropeptide VGF is Reduced in Human Bipolar Postmortem Brain and Contributes to Some of the Behavioral and Molecular Effects of Lithium
Name (type = corporate); (authority = RutgersOrg-Department)
NamePart
Neuroscience and Cell Biology
Name (type = corporate); (authority = RutgersOrg-School)
NamePart
Robert Wood Johnson Medical School (RWJMS)
Name (type = corporate); (authority = RutgersOrg-Department)
NamePart
Statistics and Biostatistics
Name (type = corporate); (authority = RutgersOrg-Department)
NamePart
School of Arts and Sciences (SAS) (New Brunswick)
Name (type = corporate); (authority = RutgersOrg-Department)
NamePart
Waksman Institute of Microbiology
Name (type = corporate); (authority = RutgersOrg-Department)
NamePart
Medicine (Robert Wood Johnson Medical School, RWJMS)-General Internal Medicine
Genre (authority = RULIB-FS)
Article, Refereed
Genre (authority = NISO JAV)
Version of Record (VoR)
Note (type = peerReview)
Peer reviewed
OriginInfo
DateIssued (encoding = w3cdtf); (qualifier = exact); (keyDate = yes)
2010
Abstract (type = Abstract)
Recent studies demonstrate that the neuropeptide VGF (non-acronymic) is regulated in the hippocampus by antidepressant therapies and animal models of depression and that acute VGF treatment has antidepressant-like activity in animal paradigms. However, the role of VGF in human psychiatric disorders is unknown. We now demonstrate using in situ hybridization that VGF is downregulated in bipolar disorder in the CA region of the hippocampus and Brodmann’s Area 9 (BA9) of the prefrontal cortex. The mechanism of VGF in relation to LiCl was explored. Both LiCl intraperitoneally (IP) and VGF intracerebroventricularly (ICV) reduced latency to drink in novelty-induced hypophagia and LiCl was not effective in VGF+/- mice suggesting that VGF may contribute to the effects of LiCl in this behavioral procedure that responds to chronic antidepressant treatment. VGF by intrahippocampal injection also had novel activity in an amphetamineinduced hyperlocomotion assay thus mimicking the actions of LiCl injected IP in a system that phenocopies manic-like behavior. Moreover, VGF+/- mice exhibited increased locomotion following amphetamine and did not respond to LiCl, suggesting that VGF is required for the effects of LiCl in curbing the response to amphetamine. Finally, VGF by ICV in vivo activated the same signaling pathways as LiCl and is necessary for the induction of MAPK and AKT by LiCl thus lending insight into the molecular mechanisms underlying the actions of VGF. The dysregulation of VGF in bipolar disorder as well as the behavioral effects of the neuropeptide similar to LiCl suggests that VGF may underlie the pathophysiology of bipolar disorder.
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English
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application/pdf
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13 p.
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DescriptiveEvent
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Citation
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2010
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The Journal of Neuroscience
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Journal
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Has part
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9368-9380
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30(28)
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https://dx.doi.org/10.1523/JNEUROSCI.5987-09.2010
Extension
DescriptiveEvent
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Grant award
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Funder
Name
National Institutes of Health
Subject (authority = LCSH)
Topic
Cellular therapy
Subject (authority = local)
Topic
Neurotrophins
Subject (authority = local)
Topic
Neurotropic factor
Subject (authority = local)
Topic
Dendritic differentiation
Subject (authority = LCSH)
Topic
Dendrites
Subject (authority = local)
Topic
Synaptogenesis
Subject (authority = LCSH)
Topic
Nerve growth factor
Name (type = personal)
NamePart (type = family)
Thakker-Varia
NamePart (type = given)
Smita
Affiliation
Neuroscience and Cell Biology, Rutgers University
Role
RoleTerm (type = text); (authority = marcrt)
author
Name (type = personal)
NamePart (type = family)
Jean
NamePart (type = given)
Ying Y.
Affiliation
Neuroscience and Cell Biology, Rutgers University
Role
RoleTerm (type = text); (authority = marcrt)
author
Name (type = personal)
NamePart (type = family)
Parikh
NamePart (type = given)
Payal
Affiliation
Medicine (Robert Wood Johnson Medical School, RWJMS)-General Internal Medicine, Rutgers University
Role
RoleTerm (type = text); (authority = marcrt)
author
Name (type = personal)
NamePart (type = family)
Sizer
NamePart (type = given)
Caroline F.
Affiliation
Neuroscience and Cell Biology, Rutgers University
Role
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author
Name (type = personal)
NamePart (type = family)
Ayer
NamePart (type = given)
Jennifer J.
Affiliation
Waksman Institute of Microbiology, Rutgers University
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author
Name (type = personal)
NamePart (type = family)
Parikh
NamePart (type = given)
Ankit
Affiliation
Neuroscience and Cell Biology, Rutgers University
Role
RoleTerm (type = text); (authority = marcrt)
author
Name (type = personal)
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Hyde
NamePart (type = given)
Thomas M.
Affiliation
National Institute of Mental Health
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author
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Buyske
NamePart (type = given)
Steven
Affiliation
Statistics and Biostatistics, Rutgers University
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RoleTerm (type = text); (authority = marcrt)
author
Name (type = personal); (authority = orcid); (authorityURI = http://id.loc.gov/vocabulary/identifiers/orcid.html); (valueURI = http://orcid.org/0000-0002-5694-4946)
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Alder
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Janet
Affiliation
Neuroscience and Cell Biology, Rutgers University
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author
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Alder, Janet
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rucore30160300001
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Thakker-Varia, Smita
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rucore30188900001
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Ayer, Jennifer J.
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rucore30194300001
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Buyske, Steven
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rucore30152500001
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Parikh, Payal
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rucore30212700001
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Identifier (type = doi)
doi:10.7282/T3R78H68
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Copyright for scholarly resources published in RUcore is retained by the copyright holder. By virtue of its appearance in this open access medium, you are free to use this resource, with proper attribution, in educational and other non-commercial settings. Other uses, such as reproduction or republication, may require the permission of the copyright holder.
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This work is available to the public to copy, distribute, or display under a Creative Commons Attribution 4.0 International (CC BY 4.0) license.
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Jean
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Caroline
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Jennifer
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Parikh
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Steven
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Janet
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2010-07-08T12:57:58
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2016-07-19T13:18:07
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