ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Behavioral and structural responses to chronic cocaine require a feedforward loop involving ΔFosB and calcium/calmodulin-dependent protein kinase II in the nucleus accumbens shell.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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Who cites it
106 citing papers in PubMed, 191 citations in OpenAlex.
- Dopamine D2 Receptors, D1/D2 Receptor Heteromers and CaMKII Signaling in the Neurobiology of Drug Addiction.Molecular neurobiology · 2026Review
- Transcriptional regulation of ventral hippocampus-nucleus accumbens circuit excitability drives cocaine seeking.Science advances · 2026Article
- Transcription factors implicated in substance use disorder, from immediate early genes to altered gene expression.Brain research · 2026Review
- Blood-brain-barrier-crossing lipid nanoparticles for mRNA delivery to the central nervous system.Nature materials · 2025Article
- The Role of ΔFosB in the Pathogenesis of Levodopa-Induced Dyskinesia: Mechanisms and Therapeutic Strategies.Molecular neurobiology · 2025Review
- Voluntary Running and Estrous Cycle Modulate ΔFOSB in the Suprachiasmatic Nucleus of the Wistar Rat.Journal of circadian rhythms · 2025Article
- Activation of the nucleus accumbens promotes place preference and counteracts stress-induced hyperthermia.iScience · 2024Article
- Exploring the potential link between ΔFosB andActa neuropsychiatrica · 2024Review
- Early-life stress and ovarian hormones alter transcriptional regulation in the nucleus accumbens resulting in sex-specific responses to cocaine.Cell reports · 2023Article
- Activation of the rostral nucleus accumbens shell by optogenetics induces cataplexy-like behavior in orexin neuron-ablated mice.Scientific reports · 2023Article
- ΔFosB is part of a homeostatic mechanism that protects the epileptic brain from further deterioration.Frontiers in molecular neuroscience · 2023Article
- Epigenetic Modulation of Opioid Receptors by Drugs of Abuse.International journal of molecular sciences · 2022Review
- A high-affinity cocaine binding site associated with the brain acid soluble protein 1.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- TAAR1 regulates drug-induced reinstatement of cocaine-seeking via negatively modulating CaMKIIα activity in the NAc.Molecular psychiatry · 2022Article
- Addiction-induced plasticity in underlying neural circuits.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Review
- ΔFOSB: A Potentially Druggable Master Orchestrator of Activity-Dependent Gene Expression.ACS chemical neuroscience · 2022Article
- Key transcription factors mediating cocaine-induced plasticity in the nucleus accumbens.Molecular psychiatry · 2022Review
- Article
- Repetitive and Inflexible Active Coping and Addiction-like Neuroplasticity in Stressed Mice of a Helplessness-Resistant Inbred Strain.Behavioral sciences (Basel, Switzerland) · 2021Article
- NLRP3 Inflammasome Is Involved in Cocaine-Mediated Potentiation on Behavioral Changes in CX3CR1-Deficient Mice.Journal of personalized medicine · 2021Article
46 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
The transcription factor ΔFosB and the brain-enriched calcium/calmodulin-dependent protein kinase II (CaMKIIα) are induced in the nucleus accumbens (NAc) by chronic exposure to cocaine or other psychostimulant drugs of abuse, in which the two proteins mediate sensitized drug responses. Although ΔFosB and CaMKIIα both regulate AMPA glutamate receptor expression and function in NAc, dendritic spine formation on NAc medium spiny neurons (MSNs), and locomotor sensitization to cocaine, no direct link between these molecules has to date been explored. Here, we demonstrate that ΔFosB is phosphorylated by CaMKIIα at the protein-stabilizing Ser27 and that CaMKII is required for the cocaine-mediated accumulation of ΔFosB in rat NAc. Conversely, we show that ΔFosB is both necessary and sufficient for cocaine induction of CaMKIIα gene expression in vivo, an effect selective for D1-type MSNs in the NAc shell subregion. Furthermore, induction of dendritic spines on NAc MSNs and increased behavioral responsiveness to cocaine after NAc overexpression of ΔFosB are both CaMKII dependent. Importantly, we demonstrate for the first time induction of ΔFosB and CaMKII in the NAc of human cocaine addicts, suggesting possible targets for future therapeutic intervention. These data establish that ΔFosB and CaMKII engage in a cell-type- and brain-region-specific positive feedforward loop as a key mechanism for regulating the reward circuitry of the brain in response to chronic cocaine.
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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.