ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Infralimbic BDNF/TrkB enhancement of GluN2B currents facilitates extinction of a cocaine-conditioned place preference.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Peripheral neurotrophin levels during controlled crack/cocaine abstinence: a systematic review and meta-analysis.Scientific reports · 2024Pooled it
- Article
- LF-DBS of the ventral striatum shortens persistence for morphine place preference and modulates BDNF expression in the hippocampus.Behavioural brain research · 2025Article
- Vagus Nerve Stimulation (VNS) Modulates Synaptic Plasticity in the Infralimbic Cortex via Trk-B Receptor Activation to Reduce Drug-Seeking in Male Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Vagus nerve stimulation (VNS) modulates synaptic plasticity in the rat infralimbic cortex via Trk-B receptor activation to reduce drug-seeking.bioRxiv : the preprint server for biology · 2024Article
- Molecular mechanisms underlying sex and treatment-dependent differences in an animal model of cue-exposure therapy for cocaine relapse prevention.Frontiers in neuroscience · 2024Article
- Inhibition of CSF1R, a receptor involved in microglia viability, alters behavioral and molecular changes induced by cocaine.Scientific reports · 2021Article
- Rottlerin, BDNF, and the impairment of inhibitory avoidance memory.Psychopharmacology · 2021Article
- Perineuronal Net Receptor PTPσ Regulates Retention of Memories.Frontiers in synaptic neuroscience · 2021Article
- Molecular and circuit mechanisms regulating cocaine memory.Cellular and molecular life sciences : CMLS · 2020Review
- Facilitative effects of environmental enrichment for cocaine relapse prevention are dependent on extinction training context and involve increased TrkB signaling in dorsal hippocampus and ventromedial prefrontal cortex.Behavioural brain research · 2020Article
- Article
- Decreased effective connection from the parahippocampal gyrus to the prefrontal cortex in Internet gaming disorder: A MVPA and spDCM study.Journal of behavioral addictions · 2020Article
- Effects of stress on the structure and function of the medial prefrontal cortex: Insights from animal models.International review of neurobiology · 2020Review
- Neuroplasticity transcript profile of the ventral striatum in the extinction of opioid-induced conditioned place preference.Neurobiology of learning and memory · 2019Article
- Accumbens brain-derived neurotrophic factor (BDNF) transmission inhibits cocaine seeking.Addiction biology · 2019Article
- Brain and Cognition for Addiction Medicine: From Prevention to Recovery Neural Substrates for Treatment of Psychostimulant-Induced Cognitive Deficits.Frontiers in psychiatry · 2019Review
- Role of prefrontal cortex in the extinction of drug memories.Psychopharmacology · 2019Review
- Cocaine-induced Changes in the Expression of NMDA Receptor Subunits.Current neuropharmacology · 2019Review
- Infralimbic Estradiol Enhances Neuronal Excitability and Facilitates Extinction of Cocaine Seeking in Female RatsFrontiers in behavioral neuroscience · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Brain-derived neurotrophic factor (BDNF) regulates synaptic activity and behavioral flexibility, and reduction of BDNF strongly predicts psychiatric disorders and cognitive dysfunction. Restoration of BDNF-dependent activity could alleviate these impairments, but BDNF has limited clinical utility due to its pharmacokinetics. Here we demonstrate that activation of a primary BDNF target, the tropomyosin-related kinase B (TrkB) receptor, enhances the amplitude and prolongs the decay kinetics of N-methyl-d-aspartate receptor (NMDAR) currents in male rat infralimbic prefrontal pyramidal neurons. Moreover, these effects were prevented and reversed by blockade of NMDARs containing the GluN2B subunit. Our results show that this signaling cascade bidirectionally regulates extinction of a cocaine-induced conditioned place preference (CPP), a task that requires behavioral flexibility. Blockade of infralimbic TrkB receptors or GluN2B-containing NMDARs disrupted consolidation of extinction of the CPP. In contrast, extinction was strengthened by potentiation of TrkB receptor activity with infralimbic infusions of BDNF or systemic injections of 7,8 dihydroxyflavone (7,8DHF), the newly synthesized TrkB receptor agonist. The 7,8DHF-induced enhancement of extinction was prevented by infralimbic infusions of a GluN2B-specific receptor antagonist, demonstrating that TrkB receptor activation enhances extinction of cocaine-CPP via GluN2B-containing NMDARs. Together, infralimbic TrkB receptor activation strengthens GluN2B-containing NMDAR currents to support extinction learning. TrkB receptor agonists would therefore be useful as pharmacological adjuncts for extinction-based therapies for treatment of psychiatric disorders associated with reduced BDNF activity.
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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.