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

Figure 1

Long-term memory formation at the neuronal level. A mechanistic simplification of how behavioral epigenetics exert molecular control of gene expression for memory formation. (a) At a neuronal level, memory consolidation requires gene expression (genes “on”), which “suprathreshold” learning events can naturally activate to result in long-term memory (LTM: long-term memory, e.g., >24 hrs). Note that this depiction is an oversimplification showing only the requirement for gene expression, however which genes are activated, the magnitude of their expression, and also the temporal dynamics of transient or sustained expression are also factors. Circles represent a single neuron with gene expression events occurring inside the cell nucleus (shaded). (b) In contrast, “subthreshold” learning events fail to induce gene expression for memory consolidation and therefore produce short-term memory (STM, e.g., <24 hrs) but not long-term memory (LTM, e.g., >24 hrs). (c) A special case exists if the threshold for induction of a long-term memory is lowered by an epigenetic manipulation like HDAC inhibition (e.g., the administration of sodium butyrate (NaBut), a nonselective general class I HDAC inhibitor). In this scenario, the “subthreshold” experience can be made to produce long-term memory. Moreover, the memory that forms is robust and persistent at longer timescales beyond the point at which natural memory would fail (see [12, 13]). Asterisk indicates enhanced LTM.

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