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Inhibition of histone deacetylase 3 via RGFP966 facilitates unusually accurate cue memory for excitatory and inhibitory cue-reward associations

Descriptive

TypeOfResource
Text
TitleInfo
Title
Inhibition of histone deacetylase 3 via RGFP966 facilitates unusually accurate cue memory for excitatory and inhibitory cue-reward associations
Name (type = personal)
NamePart (type = family)
Shang
NamePart (type = given)
Andrea
Affiliation
Psychology (New Brunswick), Rutgers University
Role
RoleTerm (type = text); (authority = marcrt)
author
Name (type = personal)
NamePart (type = family)
Bylipudi
NamePart (type = given)
Sooraz
Affiliation
Psychology (New Brunswick), Rutgers University
Role
RoleTerm (type = text); (authority = marcrt)
author
Name (type = personal); (authority = orcid); (authorityURI = http://id.loc.gov/vocabulary/identifiers/orcid.html); (valueURI = http://orcid.org/0000-0002-3633-5422)
NamePart (type = family)
Bieszczad
NamePart (type = given)
Kasia M.
Affiliation
Psychology (New Brunswick), Rutgers University
Role
RoleTerm (type = text); (authority = marcrt)
author
Name (type = corporate); (authority = RutgersOrg-Department)
NamePart
Psychology (New Brunswick)
Name (type = corporate); (authority = RutgersOrg-School)
NamePart
School of Arts and Sciences (SAS) (New Brunswick)
Genre (authority = RULIB-FS)
Article, Non-refereed
Genre (authority = NISO JAV)
Submitted manuscript under review (SMUR)
OriginInfo
DateCreated (encoding = w3cdtf); (qualifier = exact); (keyDate = yes)
2018
Abstract (type = Abstract)
Epigenetic mechanisms are key for regulating long-term memory (LTM) and are known to exert control on memory formation in multiple systems of the adult brain, including the sensory cortex. One epigenetic mechanism is chromatin modification by histone acetylation. Blocking the action of histone de-acetylases (HDACs) that normally negatively regulate LTM usually by repressing transcription, has been shown to enable memory formation. Indeed, HDAC inhibition appears to facilitate memory by altering the dynamics of gene expression events for consolidation, however less understood is how molecular-level consolidation processes alter subsequent memory for enhanced storage or retrieval. Here we used a sensory perspective to investigate from a behavioral-level whether the characteristics of memory formed with HDAC inhibitors are different from naturally-formed memory. One possibility is that HDAC-inhibition enables memory to form with greater sensory detail than normal. Because the auditory system undergoes learning-induced remodeling that provides substrates for sound-specific LTM, we aimed to identify behavioral effects of HDAC-inhibition on memory for specific sound features using a standard model of auditory associative cue-reward learning. We found that three systemic post-training treatments of an HDAC3-inhibitor (RGPF966, Abcam Inc.) in rats in the early phase of training facilitated auditory discriminative learning, and increased the specificity for acoustic frequency formed in memory of both excitatory (CS+) and inhibitory (CS-) associations for at least 2 weeks. The findings support that epigenetic mechanisms act on the sensory acuity and precision of memory, which can be revealed by studying the sensory aspects of long-term associative memory formation with HDAC inhibitors.
Language
LanguageTerm (authority = ISO 639-3:2007); (type = text)
English
PhysicalDescription
InternetMediaType
application/pdf
Extent
64 p.
Subject (authority = local)
Topic
Epigenetics
Subject (authority = local)
Topic
HDACs
Subject (authority = local)
Topic
Memory
Subject (authority = local)
Topic
Discrimination
Subject (authority = local)
Topic
Associative learning
Subject (authority = local)
Topic
Auditory
Extension
DescriptiveEvent
Type
Citation
DateTime (encoding = w3cdtf)
2018
AssociatedObject
Type
Journal
Relationship
Has part
Name
Behavioural Brain Research
RelatedItem (type = host)
TitleInfo
Title
Bieszczad, Kasia M.
Identifier (type = local)
rucore30174100001
RelatedItem (type = host)
TitleInfo
Title
Shang, Andrea
Identifier (type = local)
rucore30247500001
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier (type = doi)
doi:10.7282/T3SX6HFV
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RightsDeclaration (AUTHORITY = FS); (TYPE = [FS] statement #1); (ID = rulibRdec0004)
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.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
RightsEvent
Type
Permission or license
AssociatedObject
Type
License
Name
Multiple author license v. 1
Detail
I hereby grant to Rutgers, The State University of New Jersey (Rutgers) the non-exclusive right to retain, reproduce, and distribute the deposited work (Work) in whole or in part, in and from its electronic format, without fee. This agreement does not represent a transfer of copyright to Rutgers.Rutgers may make and keep more than one copy of the Work for purposes of security, backup, preservation, and access and may migrate the Work to any medium or format for the purpose of preservation and access in the future. Rutgers will not make any alteration, other than as allowed by this agreement, to the Work.I represent and warrant to Rutgers that the Work is my original work. I also represent that the Work does not, to the best of my knowledge, infringe or violate any rights of others.I further represent and warrant that I have obtained all necessary rights to permit Rutgers to reproduce and distribute the Work and that any third-party owned content is clearly identified and acknowledged within the Work.By granting this license, I acknowledge that I have read and agreed to the terms of this agreement and all related RUcore and Rutgers policies.
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Technical

RULTechMD (ID = TECHNICAL1)
ContentModel
Document
CreatingApplication
Version
1.7
DateCreated (point = end); (encoding = w3cdtf); (qualifier = exact)
2018-03-22T17:35:23
DateCreated (point = end); (encoding = w3cdtf); (qualifier = exact)
2018-03-22T17:35:23
ApplicationName
Acrobat Pro DC 18.11.20038
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