Sensory Cortical Plasticity Participates in the Epigenetic Regulation of Robust Memory Formation

被引:14
作者
Phan, Mimi L. [1 ]
Bieszczad, Kasia M. [1 ]
机构
[1] Rutgers State Univ, Dept Psychol, Behav & Syst Neurosci, Piscataway, NJ 08854 USA
关键词
PRIMARY AUDITORY-CORTEX; LONG-TERM-MEMORY; TEMPORAL PLASTICITY; TRANSCRIPTION FACTORS; PHYSIOLOGICAL MEMORY; HISTONE ACETYLATION; OBJECT RECOGNITION; NEGATIVE REGULATOR; CRITICAL PERIOD; MECHANISMS;
D O I
10.1155/2016/7254297
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Neuroplasticity remodels sensory cortex across the lifespan. A function of adult sensory cortical plasticity may be capturing available information during perception for memory formation. The degree of experience-dependent remodeling in sensory cortex appears to determine memory strength and specificity for important sensory signals. A key open question is how plasticity is engaged to induce different degrees of sensory cortical remodeling. Neural plasticity for long-term memory requires the expression of genes underlying stable changes in neuronal function, structure, connectivity, and, ultimately, behavior. Lasting changes in transcriptional activity may depend on epigenetic mechanisms; some of the best studied in behavioral neuroscience are DNA methylation and histone acetylation and deacetylation, which, respectively, promote and repress gene expression. One purpose of this review is to propose epigenetic regulation of sensory cortical remodeling as a mechanism enabling the transformation of significant information from experiences into content-rich memories of those experiences. Recent evidence suggests how epigenetic mechanisms regulate highly specific reorganization of sensory cortical representations that establish a widespread network for memory. Thus, epigenetic mechanisms could initiate events to establish exceptionally persistent and robust memories at a systems-wide level by engaging sensory cortical plasticity for gating what and how much information becomes encoded.
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页数:12
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