ArticleNeuron2016
Bidirectional Synaptic Structural Plasticity after Chronic Cocaine Administration Occurs through Rap1 Small GTPase Signaling.
Article in Neuron, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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Who cites it
55 citing papers in PubMed, 83 citations in OpenAlex.
- IoT-enabled wireless neural implant for chronic, programmable neuropharmacology and optogenetics.Science advances · 2026Article
- Rap1-Dependent pathways in depression: Genetic, Epigenetic, and neuroinflammatory mechanisms shaping synaptic resilience.Molecular biology reports · 2025Review
- Externalizing as a common genetic influence for a broad spectrum of substance use and behavioral conditions: A developmental perspective from the Avon Longitudinal Study of Parents and Children.Addiction (Abingdon, England) · 2025Article
- Anxiety and Beyond: Diversity in Ventral Hippocampus Circuits and Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Enhanced Rap1 small GTPase activity in the ventral hippocampus drives stress-induced anxiety.Science advances · 2025Article
- Reward integration in prefrontal-cortical and ventral-hippocampal nucleus accumbens inputs cooperatively modulates engagement.Nature communications · 2025Article
- Independent origins and non-parallel selection signatures of triclabendazole resistance in Fasciola hepatica.Nature communications · 2025Article
- Epac2-mediated synaptic insertion of CaNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- The Primary Cilia are Associated with the Axon Initial Segment in Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The biology of addiction.Science signaling · 2025Review
- Identification ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Neuronal Ensembles in the Amygdala Allow Social Information to Motivate Later Decisions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Decoding cocaine-induced proteomic adaptations in the mouse nucleus accumbens.Science signaling · 2024Article
- Stress-mediated dysregulation of the Rap1 small GTPase impairs hippocampal structure and function.iScience · 2023Article
- Bile acids modulate reinstatement of cocaine conditioned place preference and accumbal dopamine dynamics without compromising appetitive learning.Scientific reports · 2023Article
- The potential therapeutic roles of Rho GTPases in substance dependence.Frontiers in molecular neuroscience · 2023Article
- Transcriptome profiling of the ventral pallidum reveals a role for pallido-thalamic neurons in cocaine reward.Molecular psychiatry · 2022Article
- Article
- Epac2 in midbrain dopamine neurons contributes to cocaine reinforcement via enhancement of dopamine release.eLife · 2022Article
- A feature of maternal sleep apnea during gestation causes autism-relevant neuronal and behavioral phenotypes in offspring.PLoS biology · 2022Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
Dendritic spines are the sites of most excitatory synapses in the CNS, and opposing alterations in the synaptic structure of medium spiny neurons (MSNs) of the nucleus accumbens (NAc), a primary brain reward region, are seen at early versus late time points after cocaine administration. Here we investigate the time-dependent molecular and biochemical processes that regulate this bidirectional synaptic structural plasticity of NAc MSNs and associated changes in cocaine reward in response to chronic cocaine exposure. Our findings reveal key roles for the bidirectional synaptic expression of the Rap1b small GTPase and an associated local synaptic protein translation network in this process. The transcriptional mechanisms and pathway-specific inputs to NAc that regulate Rap1b expression are also characterized. Collectively, these findings provide a precise mechanism by which nuclear to synaptic interactions induce "metaplasticity" in NAc MSNs, and we reveal the specific effects of this plasticity on reward behavior in a brain circuit-specific manner.
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Registered trials
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.