ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
Calpain-GRIP Signaling in Nucleus Accumbens Core Mediates the Reconsolidation of Drug Reward Memory.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- The ventral hippocampus and nucleus accumbens as neural substrates for cocaine contextual memory reconsolidation.Translational psychiatry · 2025Article
- Roles of lncLingo2 and its derived miR-876-5p in the acquisition of opioid reinforcement.Addiction biology · 2024Article
- Drug memory reconsolidation: from molecular mechanisms to the clinical context.Translational psychiatry · 2023Review
- Plk2 promotes synaptic destabilization through disruption of N-cadherin adhesion complexes during homeostatic adaptation to hyperexcitation.Journal of neurochemistry · 2023Article
- Individual differences in cocaine-induced conditioned place preference in male rats: Behavioral and transcriptomic evidence.Journal of psychopharmacology (Oxford, England) · 2022Article
- Effects of 3-methylmethcathinone on conditioned place preference and anxiety-like behavior: Comparison with methamphetamine.Frontiers in molecular neuroscience · 2022Article
- Transcriptomic Analysis of Long Non-coding RNA-MicroRNA-mRNA Interactions in the Nucleus Accumbens Related to Morphine Addiction in Mice.Frontiers in psychiatry · 2022Article
- Glutamate receptor-interacting protein 1 in D1- and D2-dopamine receptor-expressing medium spiny neurons differentially regulates cocaine acquisition, reinstatement, and associated spine plasticity.Frontiers in cellular neuroscience · 2022Article
- Extracellular signal-regulated kinase in the basolateral amygdala is required for reconsolidation of heroin-associated memory.Frontiers in molecular neuroscience · 2022Article
- High-Frequency Deep Brain Stimulation of the Substantia Nigra Pars Reticulata Facilitates Extinction and Prevents Reinstatement of Methamphetamine-Induced Conditioned Place Preference.Frontiers in pharmacology · 2021Article
- The Mechanisms and Boundary Conditions of Drug Memory Reconsolidation.Frontiers in neuroscience · 2021Review
- Article
- Glutamate receptor interacting protein acts within the prefrontal cortex to blunt cocaine seeking.Neuropharmacology · 2019Article
- Reconsolidation blockade for the treatment of addiction: challenges, new targets, and opportunities.Learning & memory (Cold Spring Harbor, N.Y.) · 2018Review
- Potential Alzheimer's Disease Therapeutics Among Weak Cysteine Protease Inhibitors Exhibit Mechanistic Differences Regarding Extent of Cathepsin B Up-Regulation and Ability to Block Calpain.European scientific journal · 2017Article
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Authors and funding
11 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to drug-paired cues causes drug memories to be in a destabilized state and interfering with memory reconsolidation can inhibit relapse. Calpain, a calcium-dependent neutral cysteine protease, is involved in synaptic plasticity and the formation of long-term fear memory. However, the role of calpain in the reconsolidation of drug reward memory is still unknown. In the present study, using a conditioned place preference (CPP) model, we found that exposure to drug-paired contextual stimuli induced the activation of calpain and decreased the expression of glutamate receptor interacting protein 1 (GRIP1) in the nucleus accumbens (NAc) core, but not shell, of male rats. Infusions of calpain inhibitors in the NAc core immediately after retrieval disrupted the reconsolidation of cocaine/morphine cue memory and blocked retrieval-induced calpain activation and GRIP1 degradation. The suppressive effect of calpain inhibitors on the expression of drug-induced CPP lasted for at least 14 d. The inhibition of calpain without retrieval 6 h after retrieval or after exposure to an unpaired context had no effects on the expression of reward memory. Calpain inhibition after retrieval also decreased cocaine seeking in a self-administration model and this effect did not recover spontaneously after 28 d. Moreover, the knock-down of GRIP1 expression in the NAc core by lentivirus-mediated short-hairpin RNA blocked disruption of the reconsolidation of drug cue memories that was induced by calpain inhibitor treatment. These results suggest that calpain activity in the NAc core is crucial for the reconsolidation of drug reward memory via the regulation of GRIP1 expression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.