Research ReportVariation in the persistence of memory: An interplay between actin dynamics and AMPA receptors

- Some variation in the persistence of can be explained by the biochemistry of dendritic spines.
- Generating short-term memory requires degrading actin and trafficking GluA1 AMPA receptors into the post-synaptic density.
- The threshold for producing these events is low but the underlying synaptic changes will not persist.
- To persist the actin cytoskeleton must be rebuilt and GluA1 AMPA receptors must be replaced with GluA2 containing receptors.
- The stabilization of an enlarged actin cytoskeleton is the target outcome that consolidates the synaptic basis of memory.

William James noted that memories could persist from minutes to weeks. This essay attempts to explain this variation by situating the explanation in the biochemistry of dendritic spines. Two outcomes are critical to generate the synaptic basis of memory: (1) the actin cytoskeleton in the spine must be degraded to permit (2) additional AMPA receptors (GluA1s) to enter new “hot spots” in the postsynaptic density. These initial outcomes can support short-lasting memories. The threshold for these events is low but the underlying synaptic changes cannot resist the endocytic processes that remove the added AMPA receptors. For the memory to persist the degraded actin cytoskeleton must be rebuilt and the vacated “hot spots” refilled with GluA2 receptors. A primary claim is that it is the stabilization of an enlarged actin cytoskeleton that is the target outcome that consolidates the synaptic basis of memory (see Lynch et al., 2007). The stabilized actin cytoskeleton has properties that enable it to garner the synaptic proteins it needs to self sustain the potentiated state and to benefit from activation of memory modulation systems.This article is part of a Special Issue entitled Brain and Memory.