ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
BDNF interacts with endocannabinoids to regulate cocaine-induced synaptic plasticity in mouse midbrain dopamine neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- FAAH and MAGL inhibition: Evolving approaches to treating substance use disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Review
- Article
- BDNF Activates Postsynaptic TrkB Receptors to Induce Endocannabinoid Release and Inhibit Presynaptic Calcium Influx at a Calyx-Type Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Activation of tyrosine phosphatase PTP1B in pyramidal neurons impairs endocannabinoid signaling by tyrosine receptor kinase trkB and causes schizophrenia-like behaviors in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Astroglia-Derived BDNF and MSK-1 Mediate Experience- and Diet-Dependent Synaptic Plasticity.Brain sciences · 2020Article
- Gut Microbiota Regulates Depression-Like Behavior in Rats Through the Neuroendocrine-Immune-Mitochondrial Pathway.Neuropsychiatric disease and treatment · 2020Article
- Lights on Endocannabinoid-Mediated Synaptic Potentiation.Frontiers in molecular neuroscience · 2020Review
- Increased levels of synaptic proteins involved in synaptic plasticity after chronic intraocular pressure elevation and modulation by brain-derived neurotrophic factor in a glaucoma animal model.Disease models & mechanisms · 2019Article
- Article
- Endogenous cannabinoids mediate the effect of BDNF at CA1 inhibitory synapses in the hippocampus.Synapse (New York, N.Y.) · 2018Article
- HCN2 channels in the ventral tegmental area regulate behavioral responses to chronic stress.eLife · 2018Article
- Brain-Derived Neurotrophic Factor (BDNF) Role in Cannabinoid-Mediated Neurogenesis.Frontiers in cellular neuroscience · 2018Article
- Resveratrol modulates cocaine-induced inhibitory synaptic plasticity in VTA dopamine neurons by inhibiting phosphodiesterases (PDEs).Scientific reports · 2017Article
- Endocannabinoid modulation of dopamine neurotransmission.Neuropharmacology · 2017Review
- PDE4 Inhibition Restores the Balance Between Excitation and Inhibition in VTA Dopamine Neurons Disrupted by Repeated In Vivo Cocaine Exposure.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- BDNF-induced endocannabinoid release modulates neocortical glutamatergic neurotransmission.Synapse (New York, N.Y.) · 2017Article
- Genome-wide analysis of the nucleus accumbens identifies DNA methylation signals differentiating low/binge from heavy alcohol drinking.Alcohol (Fayetteville, N.Y.) · 2017Article
- The Epac-Phospholipase Cε Pathway Regulates Endocannabinoid Signaling and Cocaine-Induced Disinhibition of Ventral Tegmental Area Dopamine Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Drug-Induced Alterations of Endocannabinoid-Mediated Plasticity in Brain Reward Regions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Review
- Fluoxetine Facilitates Fear Extinction Through Amygdala Endocannabinoids.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Brain-derived neurotrophic factor (BDNF) and endocannabinoids (eCBs) have been individually implicated in behavioral effects of cocaine. The present study examined how BDNF-eCB interaction regulates cocaine-induced synaptic plasticity in the ventral tegmental area and behavioral effects. We report that BDNF and selective tyrosine kinase receptor B (TrkB) agonist 7,8-dihydroxyflavone (DHF) activated the TrkB receptor to facilitate two forms of eCB-mediated synaptic depression, depolarization-induced suppression of inhibition (DSI), and long-term depression (I-LTD) of IPSCs in ventral tegmental area dopamine neurons in mouse midbrain slices. The facilitation appears to be mediated by an increase in eCB production via phospholipase Cγ pathway, but not by an increase in CB1 receptor responsiveness or a decrease in eCB hydrolysis. Using Cre-loxP technology to specifically delete BDNF in dopamine neurons, we showed that eCB-mediated I-LTD, cocaine-induced reduction of GABAergic inhibition, and potentiation of glutamatergic excitation remained intact in wild-type control mice, but were impaired in BDNF conditional knock-out mice. We also showed that cocaine-induced conditioned place preference was attenuated in BDNF conditional knock-out mice, in vivo pretreatments with DHF before place conditioning restored cocaine conditioned place preference in these mice, and the behavioral effect of DHF was blocked by a CB₁ receptor antagonist. Together, these results suggest that BDNF in dopamine neurons regulates eCB responses, cocaine-induced synaptic plasticity, and associative learning.
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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.