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A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration

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Published on: January 22, 2016

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

Erica J Young¹, Massimiliano Aceti², Erica M Griggs¹

¹Department of Metabolism and Aging, The Scripps Research Institute, Jupiter, Florida; Department of Neuroscience, The Scripps Research Institute, Jupiter, Florida.

Biological Psychiatry

|September 10, 2013

Summary

This summary is machine-generated.

Drug-associated memories, like those formed with methamphetamine, are actively maintained by cycling actin and myosin II. Inhibiting this process can disrupt these memories, offering a potential therapeutic target for addiction.

Keywords:

Addiction amygdala dendritic spine memory maintenance myosin structural plasticity

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Area of Science:

Neuroscience
Molecular Biology
Addiction Research

Background:

Drug addiction is linked to memories that increase relapse risk.
Memory consolidation involves F-actin polymerization in synapses.
Mechanisms for long-term memory maintenance are not fully understood.

Purpose of the Study:

To investigate the role of F-actin polymerization and myosin II in maintaining methamphetamine-associated memories.
To explore the structural plasticity underlying these memories.

Main Methods:

Used conditioned place preference and context-induced reinstatement models.
Administered a specific actin cycling inhibitor and inhibited non-muscle myosin II in the amygdala.

Main Results:

Methamphetamine-associated memories, but not those from foot shock or food, were disrupted by actin inhibition post-consolidation.
This disruption was immediate, persistent, and independent of memory retrieval or strength.
Inhibition of non-muscle myosin II also impaired methamphetamine-associated memory.

Conclusions:

Drug-associated memories are actively maintained by a unique F-actin and myosin II-driven process.
This suggests a potential therapeutic strategy for selectively treating unwanted drug memories without retrieval.
Memory maintenance appears dependent on preserving polymerized actin.