ArticleScientific reports2017
AMPK signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Therapeutic effects of metformin on cocaine conditioned place preference and locomotion.Behavioral neuroscience · 2025Article
- Disrupting heroin-associated memory reconsolidation through actin polymerization inhibition in the nucleus accumbens core.The international journal of neuropsychopharmacology · 2024Article
- Effects of metformin on binge-like ethanol drinking and adenosine monophosphate kinase signaling in inbred high drinking in the dark line 1 mice.Alcohol, clinical & experimental research · 2024Article
- Metformin Prevents Cocaine Sensitization: Involvement of Adenosine Monophosphate-Activated Protein Kinase Trafficking between Subcellular Compartments in the Corticostriatal Reward Circuit.International journal of molecular sciences · 2023Article
- Metformin in nucleus accumbens core reduces cue-induced cocaine seeking in male and female rats.Addiction biology · 2022Article
- Identification of miRNA-mediated gene regulatory networks in L-methionine exposure counteracts cocaine-conditioned place preference in mice.Frontiers in genetics · 2022Article
- Influence of psychostimulants and opioids on epigenetic modification of class III histone deacetylase (HDAC)-sirtuins in glial cells.Scientific reports · 2021Article
- Stress-induced alterations of mesocortical and mesolimbic dopaminergic pathways.Scientific reports · 2021Article
- Kinase network dysregulation in a human induced pluripotent stem cell model of DISC1 schizophrenia.Molecular omics · 2019Article
- Protein Translation in the Nucleus Accumbens Is Dysregulated during Cocaine Withdrawal and Required for Expression of Incubation of Cocaine Craving.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Relapse to drug seeking can be caused by exposure to drug-associated cues, provoking drug craving even after prolonged abstinence. Recent studies demonstrated that AMP-activated protein kinase (AMPK) regulates neuronal morphology and membrane excitability in neurons. Here, we investigated the role of AMPK activity in the nucleus accumbens (NAc) in relapse to cocaine seeking. We found that exposure to drug-related cues reinstated cocaine-seeking behavior and increased AMPK and p70s6k phosphorylation in the NAc core but not shell. Augmenting AMPK activity by intra-NAc core infusions of the AMPK activator 5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide (AICAR) or adenovirus expressing constitutively active subunits of AMPK decreased cue-induced reinstatement of cocaine seeking and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal-regulated kinase 1/2 (ERK1/2) pathways. In contrast, inhibition of AMPK activity by intra-NAc core infusions of the AMPK inhibitor compound C or adenovirus expressing dominant-negative subunits of AMPK increased cue-induced reinstatement of cocaine seeking and enhanced mTORC1 and ERK1/2 activity. The regulation of AMPK activity in the NAc shell had no effect on cue-induced cocaine seeking. Altogether, these results indicate that AMPK activity in the NAc core is critical for the cue-induced reinstatement of cocaine seeking, which may be mediated by mTORC1 and ERK1/2 signaling.
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