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

Figure 2

Long-term memory formation at a systems level. A schematic showing how a learning event can lead to two different outcomes for long-term memory when considering populations of neurons. (a) Learning processes can target a population of neurons that process task-dependent information during an experience. A typical threshold for long-term memory induction may only achieve gene expression events in a small number of neurons (here, only one out of the possible seven representatives of the population) that will undergo plasticity for memory consolidation and the formation of LTM. (b) If the threshold for memory induction is lower, gene expression events may occur in more neurons (here, five out of the seven neurons). The recruitment of more neurons with plasticity engaged could induce a larger network for memory that persists beyond typical long-term memory timescales. Notably, this conceptualization is applicable to any case of unusually strong and robust memories, including those induced by experimental manipulations (e.g., HDAC inhibition) and environmental influences such as stress, disease, drugs of abuse, or even therapeutic cognitive training paradigms. Conventions are as in Figure 1.

(a)

(b)