ArticleProceedings of the National Academy of Sciences of the United States of America2017
BDNF-TrkB controls cocaine-induced dendritic spines in rodent nucleus accumbens dissociated from increases in addictive behaviors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- eIF4E-Dependent Translation Potentially Regulates Apoptosis and BDNF/TrkB Signaling in the Medial Prefrontal Cortex During Morphine-Induced CPP.International journal of molecular sciences · 2026Article
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- Abuse Potential and Neurotoxic Effects of the Synthetic Cannabinoid 4F-ABUTINACA Self-Administration in Adult Male Rats.Addiction biology · 2026Article
- The ventral hippocampus and nucleus accumbens as neural substrates for cocaine contextual memory reconsolidation.Translational psychiatry · 2025Article
- Phytochemicals Targeting BDNF Signaling for Treating Neurological Disorders.Brain sciences · 2025Review
- Exploring α-synuclein Interaction Partners and their Potential Clinical Implications for Parkinson's Disease.Neurochemical research · 2024Article
- Article
- miRNA signatures associated with vulnerability to food addiction in mice and humans.The Journal of clinical investigation · 2022Article
- More than Addiction-The Nucleus Accumbens Contribution to Development of Mental Disorders and Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Epigenetic Effects of Addictive Drugs in the Nucleus Accumbens.Frontiers in molecular neuroscience · 2022Review
- Neuroplasticity and Multilevel System of Connections Determine the Integrative Role of Nucleus Accumbens in the Brain Reward System.International journal of molecular sciences · 2021Review
- Inhibition of CSF1R, a receptor involved in microglia viability, alters behavioral and molecular changes induced by cocaine.Scientific reports · 2021Article
- A growth-factor-activated lysosomal KNature · 2021Article
- Pleasure, addiction, and hypocretin (orexin).Handbook of clinical neurology · 2021Review
- AddictGene: An integrated knowledge base for differentially expressed genes associated with addictive substance.Computational and structural biotechnology journal · 2021Article
- Endocannabinoid signaling regulates the reinforcing and psychostimulant effects of ketamine in mice.Nature communications · 2020Article
- BDNF signaling during the lifetime of dendritic spines.Cell and tissue research · 2020Review
- Neurochemical and behavioral comparisons of contingent and non-contingent methamphetamine exposure following binge or yoked long-access self-administration paradigms.Psychopharmacology · 2020Article
- A potential role for microglia in stress- and drug-induced plasticity in the nucleus accumbens: A mechanism for stress-induced vulnerability to substance use disorder.Neuroscience and biobehavioral reviews · 2019Review
- Accumbens brain-derived neurotrophic factor (BDNF) transmission inhibits cocaine seeking.Addiction biology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
Chronic cocaine use is associated with prominent morphological changes in nucleus accumbens shell (NACsh) neurons, including increases in dendritic spine density along with enhanced motivation for cocaine, but a functional relationship between these morphological and behavioral phenomena has not been shown. Here we show that brain-derived neurotrophic factor (BDNF) signaling through tyrosine kinase B (TrkB) receptors in NACsh neurons is necessary for cocaine-induced dendritic spine formation by using either localized TrkB knockout or viral-mediated expression of a dominant negative, kinase-dead TrkB mutant. Interestingly, augmenting wild-type TrkB expression after chronic cocaine self-administration reverses the sustained increase in dendritic spine density, an effect mediated by TrkB signaling pathways that converge on extracellular regulated kinase. Loss of TrkB function after cocaine self-administration, however, leaves spine density intact but markedly enhances the motivation for cocaine, an effect mediated by specific loss of TrkB signaling through phospholipase Cgamma1 (PLCγ1). Conversely, overexpression of PLCγ1 both reduces the motivation for cocaine and reverses dendritic spine density, suggesting a potential target for the treatment of addiction in chronic users. Together, these findings indicate that BDNF-TrkB signaling both mediates and reverses cocaine-induced increases in dendritic spine density in NACsh neurons, and these morphological changes are entirely dissociable from changes in addictive behavior.
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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.