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Inhibition of histone deacetylase 3 via RGFP966 facilitates exceptionally specific and enduring memory for excitatory and inhibitory sound-signal associations
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Shang, Andrea. Inhibition of histone deacetylase 3 via RGFP966 facilitates exceptionally specific and enduring memory for excitatory and inhibitory sound-signal associations. Retrieved from https://doi.org/doi:10.7282/T35M68W3

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TitleInhibition of histone deacetylase 3 via RGFP966 facilitates exceptionally specific and enduring memory for excitatory and inhibitory sound-signal associations
NameShang, Andrea (author); Bieszczad, Kasia (chair); Rutgers University; School of Graduate Studies
Date Created2018
Other Date2018-01 (degree)
SubjectPsychology, Learning, Memory
Extent1 online resource (vi, 47 p. : ill.)
DescriptionEpigenetic mechanisms that modulate gene expression are key to regulating long-term memory (LTM) formation, and are known to exert control on memory formation in multiple systems of the adult brain, including the sensory cortex. Chromatin modifications have been shown to have powerful effects on experience-dependent transcription for neuroplasticity underlying memory processes. One mechanism for chromatin modification is histone acetylation. Histone acetyltransferases (HATs) generally facilitate LTM formation by promoting gene expression, while histone deacetylases (HDACs) tend to have gene silencing effects, and negatively regulate LTM. Thus, blocking the action of HDACs has been shown to facilitate LTM formation. Because sensory cortex undergoes learning-induced remodeling over a lifetime, here we aimed to identify the ways in which HDAC-inhibition acts to facilitate LTM using a standard model of auditory memory and cortical plasticity. Auditory cortical plasticity in particular has been extensively studied in learning and memory processes. Representational plasticity in primary auditory cortex (A1) is known to reflect the formation of strong and sound-selective associative memory for behaviorally relevant sound features. In this present study, we used RGFP966, a class I HDAC inhibitor with selectivity for HDAC3 that has been shown to modulate associative learning-induced A1 plasticity (Bieszczad et al., 2015), to facilitate memory consolidation in rats learning a 2-tone sound frequency discrimination (2TD) task. We found that systemic treatments of the HDAC3-inhibitor early in 2TD task training facilitated associative learning for both excitatory (CS+) and inhibitory (CS-) sound signals, and altered the LTM formed in two ways that were independent of the final performance level achieved, which was equivalent between groups. We found that HDAC3-inhibition enhanced memory specificity for the sound-frequency of the two pure-tone CS cues, and strengthened memory for the excitatory and inhibitory sound-specific associations. Moreover, the behavioral effects of an initial, limited bout of HDAC3-inhibitor were long-lasting, enduring for at least weeks following the last administration of RGFP966. The present results support a role for HDAC3 during auditory memory consolidation by regulating the specificity and strength of newly learned sound-signal associations. This conclusion complements existing research on the effects of HDAC-inhibitors by providing a potential behavioral explanation for long-term memory enhancements.
NoteM.S.
NoteIncludes bibliographical references
Noteby Andrea Shang
Genretheses, ETD graduate
Persistent URLhttps://doi.org/doi:10.7282/T35M68W3
Languageeng
CollectionSchool of Graduate Studies Electronic Theses and Dissertations
Organization NameRutgers, The State University of New Jersey
RightsThe author owns the copyright to this work.
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