Priority CommunicationSelective, Retrieval-Independent Disruption of Methamphetamine-Associated Memory by Actin Depolymerization
Section snippets
Animals
Adult male Sprague-Dawley rats (300–350 g; Charles River, Wilmington, Massachusetts) and Thy1-GFP(m) mice (10 weeks) were housed under a 12:12 light/dark cycle, with food and water ad libitum. All procedures were performed in accordance with the Scripps Research Institutional Animal Care and Use Committee. Animals were handled for 3–5 days before behavioral conditioning.
Surgery
Rats and mice received implantation with 26G bilateral stainless steel guide cannulae directed at the BLC, and rats received
Maintenance of METH-Associated Memory Is Supported in the Amygdala by a Dynamic Actin Cytoskeleton
For CPP, animals were trained to associate the rewarding effects of METH with the multi-modal environmental context in which it was administered. Two days after training that produced a lasting memory for the METH-paired context (CS+), rats were given a single intra-BLC infusion of LatA, a highly-specific inhibitor of cycling but not stable actin (60). Fifteen minutes after infusion, METH-associated memory was assessed in the absence of the unconditioned stimulus (US), METH reinforcement (
Discussion
In this study, we demonstrate that METH-associated memory can be disrupted through direct actin depolymerization or myosin II inhibition days to weeks after consolidation, in the absence of retrieval. This rapid and persistent disruption of a memory by targeting cycling F-actin after consolidation was unexpected. We and others have previously demonstrated that learning triggers a brief window of F-actin dynamics, such that depolymerization at the time of training prevents the consolidation of
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2020, NeuropharmacologyCitation Excerpt :The insular cortex (IC) had their post-synaptic density enlarged after training in the conditioned taste aversion task (CTA); while latrunculin A administered intra-IC impaired the acquisition and consolidation of CTA (Bi et al., 2010). Drug-associated memories are impaired by intra-amygdala administration of latrunculin A (Young et al., 2014). Furthermore, post-training intra-hippocampal latrunculin A impaired contextual fear memory acquisition and extinction (Fisher et al., 2014).