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 Resjournal_title
Brain researchauthors
Rudy JWdoi
10.1016/j.brainres.2014.12.009subject
Has Abstractpub_date
2015-09-24 00:00:00pages
29-37eissn
0006-8993issn
1872-6240pii
S0006-8993(14)01678-3journal_volume
1621pub_type
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