blister and Memory-Disorders

blister has been researched along with Memory-Disorders* in 1 studies

Other Studies

1 other study(ies) available for blister and Memory-Disorders

Article	Year
Memory disrupting effects of nonmuscle myosin II inhibition depend on the class of abused drug and brain region. Learning & memory (Cold Spring Harbor, N.Y.), 2017, Volume: 24, Issue:2 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. Topics: Analysis of Variance; Anesthetics, Local; Animals; Brain; Central Nervous System Stimulants; Cocaine; Conditioning, Operant; Dendritic Spines; Green Fluorescent Proteins; Heterocyclic Compounds, 4 or More Rings; Memory Disorders; Mental Recall; Methamphetamine; Mice; Mice, Inbred C57BL; Mice, Transgenic; Microinjections; Morphine Derivatives; Myosin Type II	2017

Article

Year

Memory disrupting effects of nonmuscle myosin II inhibition depend on the class of abused drug and brain region.

Learning & memory (Cold Spring Harbor, N.Y.), 2017, Volume: 24, Issue:2

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.

Topics: Analysis of Variance; Anesthetics, Local; Animals; Brain; Central Nervous System Stimulants; Cocaine; Conditioning, Operant; Dendritic Spines; Green Fluorescent Proteins; Heterocyclic Compounds, 4 or More Rings; Memory Disorders; Mental Recall; Methamphetamine; Mice; Mice, Inbred C57BL; Mice, Transgenic; Microinjections; Morphine Derivatives; Myosin Type II

2017