Variation in the persistence of memory: An interplay between actin dynamics and AMPA receptors.

Abstract:

: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.

journal_name

Brain Res

journal_title

Brain research

authors

Rudy JW

doi

10.1016/j.brainres.2014.12.009

subject

Has Abstract

pub_date

2015-09-24 00:00:00

pages

29-37

eissn

0006-8993

issn

1872-6240

pii

S0006-8993(14)01678-3

journal_volume

1621

pub_type

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