ArticlePsychopharmacology2014
Reactivation of cocaine reward memory engages the Akt/GSK3/mTOR signaling pathway and can be disrupted by GSK3 inhibition.
Article in Psychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 80 citations in OpenAlex.
- Exercise modulates food reward: neurobiological mechanisms and implications for weight management.Frontiers in nutrition · 2026Review
- The ventral hippocampus and nucleus accumbens as neural substrates for cocaine contextual memory reconsolidation.Translational psychiatry · 2025Article
- Xenon gas as a potential treatment for opioid use disorder, alcohol use disorder, and related disorders.Medical gas research · 2025Review
- A Selective GSK3β Inhibitor, Tideglusib, Decreases Intermittent Access and Binge Ethanol Self-Administration in C57BL/6J Mice.Addiction biology · 2025Article
- Inhibition of ERK1/2 or CRMP2 Disrupts Alcohol Memory Reconsolidation and Prevents Relapse in Rats.International journal of molecular sciences · 2024Article
- Advances in fear memory erasure and its neural mechanisms.Frontiers in neurology · 2024Review
- Drug memory reconsolidation: from molecular mechanisms to the clinical context.Translational psychiatry · 2023Review
- Dopamine D3 Receptor Modulates Akt/mTOR and ERKInternational journal of molecular sciences · 2023Article
- Effects of heroin self-administration and forced withdrawal on the expression of genes related to the mTOR network in the basolateral complex of the amygdala of male Lewis rats.Psychopharmacology · 2022Article
- Molecular Mechanisms Underlying the Retrieval and Extinction of Morphine Withdrawal-Associated Memories in the Basolateral Amygdala and Dentate Gyrus.Biomedicines · 2022Article
- Anxiety and cognitive-related effects of ΔPsychopharmacology · 2022Article
- Inhibition of Glycogen Synthase Kinase 3β Activity in the Basolateral Amygdala Disrupts Reconsolidation and Attenuates Heroin Relapse.Frontiers in molecular neuroscience · 2022Article
- Mu-opioid receptor and receptor tyrosine kinase crosstalk: Implications in mechanisms of opioid tolerance, reduced analgesia to neuropathic pain, dependence, and reward.Frontiers in systems neuroscience · 2022Review
- Reactivation of cocaine contextual memory engages mechanistic target of rapamycin/S6 kinase 1 signaling.Frontiers in pharmacology · 2022Article
- Decrease of glycogen synthase kinase 3β phosphorylation in the rat nucleus accumbens shell is necessary for amphetamineinduced conditioned locomotor activity.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Akt and its phosphorylation in nucleus accumbens mediate heroin-seeking behavior induced by cues in rats.Addiction biology · 2021Article
- Chronic phenmetrazine treatment promotes DBrain research · 2021Article
- Molecular and circuit mechanisms regulating cocaine memory.Cellular and molecular life sciences : CMLS · 2020Review
- Glycogen synthase kinase-3 signaling in cellular and behavioral responses to psychostimulant drugs.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Glycogen Synthase Kinase 3β in the Ventral Hippocampus is Important for Cocaine Reward and Object Location Memory.Neuroscience · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
rationalMemories return to a labile state following their retrieval and must undergo a process of reconsolidation to be maintained. Thus, disruption of cocaine reward memories by interference with reconsolidation may be therapeutically beneficial in the treatment of cocaine addiction.
objectiveThe objectives were to elucidate the signaling pathway involved in reconsolidation of cocaine reward memory and to test whether targeting this pathway could disrupt cocaine-associated contextual memory.
methodsUsing a mouse model of conditioned place preference, regulation of the activity of glycogen synthase kinase-3 (GSK3), mammalian target of Rapamycin complex 1 (mTORC1), P70S6K, β-catenin, and the upstream signaling molecule Akt, was studied in cortico-limbic-striatal circuitry after re-exposure to an environment previously paired with cocaine.
resultLevels of phosporylated Akt-Thr308, GSK3α-Ser21, GSK3β-Ser9, mTORC1, and P70S6K were reduced in the nucleus accumbens and hippocampus 10 min after the reactivation of cocaine cue memories. Levels of pAkt and pGSK3 were also reduced in the prefrontal cortex. Since reduced phosphorylation of GSK3 indicates heightened enzyme activity, the effect of a selective GSK3 inhibitor, SB216763, on reconsolidation was tested. Administration of SB216763 immediately after exposure to an environment previously paired with cocaine abrogated a previously established place preference, suggesting that GSK3 inhibition interfered with reconsolidation of cocaine-associated reward memories.
conclusionsThese findings suggest that the Akt/GSK3/mTORC1 signaling pathway in the nucleus accumbens, hippocampus, and/or prefrontal cortex is critically involved in the reconsolidation of cocaine contextual reward memory. Inhibition of GSK3 activity during memory retrieval can erase an established cocaine place preference.
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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.