Selective, retrieval-independent disruption of methamphetamine-associated memory by actin depolymerization.

ABSTRACT:

Background

Memories associated with drugs of abuse, such as methamphetamine (METH), increase relapse vulnerability to substance use disorder. There is a growing consensus that memory is supported by structural and functional plasticity driven by F-actin polymerization in postsynaptic dendritic spines at excitatory synapses. However, the mechanisms responsible for the long-term maintenance of memories, after consolidation has occurred, are largely unknown.

Methods

Conditioned place preference (n = 112) and context-induced reinstatement of self-administration (n = 19) were used to assess the role of F-actin polymerization and myosin II, a molecular motor that drives memory-promoting dendritic spine actin polymerization, in the maintenance of METH-associated memories and relate

SUBMITTER: Young EJ 

PROVIDER: S-EPMC4023488 | biostudies-literature | 2014 Jan

REPOSITORIES: biostudies-literature