ArticlePsychopharmacology2019
Phosphoproteomic analysis of cocaine memory extinction and reconsolidation in the nucleus accumbens.
Article in Psychopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Social hierarchy modulates drug reinforcement and protein phosphorylation in the nucleus accumbens.Frontiers in pharmacology · 2025Article
- A complex of the lipid transport ER proteins TMEM24 and C2CD2 with band 4.1 at cell-cell contacts.The Journal of cell biology · 2024Article
- Phosphorylation of the nuclear poly(A) binding protein (PABPN1) during mitosis protects mRNA from hyperadenylation and maintains transcriptome dynamics.Nucleic acids research · 2024Article
- Role of Rab10 in cocaine-induced behavioral effects is associated with GABAB receptor membrane expression in the nucleus accumbens.Frontiers in pharmacology · 2024Article
- The CaMKII-dependent phosphorylation of GABACNS neuroscience & therapeutics · 2023Article
- Reactivation of cocaine contextual memory engages mechanistic target of rapamycin/S6 kinase 1 signaling.Frontiers in pharmacology · 2022Article
- Molecular and circuit mechanisms regulating cocaine memory.Cellular and molecular life sciences : CMLS · 2020Review
- Molecular Plasticity of the Nucleus Accumbens Revisited-Astrocytic Waves Shall Rise.Molecular neurobiology · 2019Review
- Editorial: the psychopharmacology of extinction-from theory to therapy.Psychopharmacology · 2019Article
- Regulation of Garcinol on Histone Acetylation in the Amygdala and on the Reconsolidation of a Cocaine-Associated Memory.Frontiers in behavioral neuroscience · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleEnvironmental stimuli, or cues, associated with the use of drugs such as cocaine are one of the primary drivers of relapse. Thus, identifying mechanisms to reduce the motivational properties of drug cues is an important research goal.
objectivesThe purpose of this study was to identify cellular signaling events in the nucleus accumbens (NAc) that are induced when a cocaine cue memory is either extinguished through repeated cue presentation in the absence of drug, or when the memory is reactivated and reconsolidated by a brief cue re-exposure. Signaling events specific to extinction or reconsolidation represent potential targets for pharmacotherapeutics that may enhance extinction or disrupt reconsolidation to reduce the likelihood of relapse.
methodsMale Sprague-Dawley rats were trained to self-administer cocaine paired with an audiovisual cue. Following a period of self-administration, the memory for the cocaine-associated cue was either extinguished, reactivated, or not manipulated (control) 15 min before sacrifice. Tissue from the NAc was subsequently analyzed using mass spectrometry based phosphoproteomics to identify cellular signaling events induced by each condition.
resultsExtinction and reconsolidation of the cocaine cue memory produced both common and distinct changes in protein phosphorylation. Notably, there were no significant changes in protein phosphorylation that were modulated in the opposite direction by the two behavioral conditions. Comparison of NAc phosphoproteomic changes to previously identified changes in the basolateral amygdala (BLA) revealed that cue extinction increases phosphorylation at serine (S) 883 of the GABA
conclusionsPhosphoproteomics is a useful tool for identifying signaling cascades involved in different memory processes and revealed novel potential targets for selectively targeting extinction versus reconsolidation of a cocaine cue memory. Furthermore, cross region analysis suggests that cue extinction may produce unique signaling events associated with increased inhibitory signaling.
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