Memory disrupting effects of nonmuscle myosin II inhibition depend on the class of abused drug and brain region
- Sherri B. Briggs1,2,3,
- Ashley M. Blouin1,2,3,
- Erica J. Young1,2,
- Gavin Rumbaugh2 and
- Courtney A. Miller1,2
- 1Department of Metabolism & Aging, The Scripps Research Institute, Jupiter, Florida 33458, USA
- 2Department of Neuroscience, The Scripps Research Institute, Jupiter, Florida 33458, USA
- Corresponding author: cmiller{at}scripps.edu
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↵3 These authors contributed equally to this work.
Abstract
Depolymerizing actin in the amygdala through nonmuscle myosin II inhibition (NMIIi) produces a selective, lasting, and retrieval-independent disruption of the storage of methamphetamine-associated memories. Here we report a similar disruption of memories associated with amphetamine, but not cocaine or morphine, by NMIIi. Reconsolidation appeared to be disrupted with cocaine. Unlike in the amygdala, methamphetamine-associated memory storage was not disrupted by NMIIi in the hippocampus, nucleus accumbens, or orbitofrontal cortex. NMIIi in the hippocampus did appear to disrupt reconsolidation. Identification of the unique mechanisms responsible for NMII-mediated, amygdala-dependent disruption of memory storage associated with the amphetamine class may enable induction of retrieval-independent vulnerability to other pathological memories.
Footnotes
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[Supplemental material is available for this article.]
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Article is online at http://www.learnmem.org/cgi/doi/10.1101/lm.043976.116.
- Received September 8, 2016.
- Accepted November 23, 2016.
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