Memory disrupting effects of nonmuscle myosin II inhibition depend on the class of abused drug and brain region
Year: 2017
Type: preprint
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.
Source: Learning & Memory
Institution: Scripps Research Institute
Language: English
Topic: Memory and Neural Mechanisms
Subfield: Cognitive Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: hybrid
Awards: MicroRNA-mediated mechanisms of social stress-potentiated drug seeking, Synaptic actin dynamics and the selective vulnerability of drug-associated memory, Evaluation of novel biomarkers of cognition in a model of sporadic developmental brain disorders and their application in efficacy testing of Ras pathway inhibitors, G8319311484
OpenAlex ID: W2575199265