ArticleNeurobiology of learning and memory2009
BDNF-induced synaptic delivery of AMPAR subunits is differentially dependent on NMDA receptors and requires ERK.
Article in Neurobiology of learning and memory, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 60 citations in OpenAlex.
- Molecular architects of memory: BDNF/TrkB signaling and trafficking in neuronal plasticity and memory.Molecular psychiatry · 2026Review
- BDNF Signaling in Glutamatergic Neurons During Long-Term Potentiation (LTP): A Spatio-Temporal Exploration of Events.Molecular neurobiology · 2025Review
- Anxiolytic reversal of classically conditioned / chronic stress-induced gene expression and learning in the Stress Alternatives Model.Behavioural brain research · 2023Article
- Regulation of AMPA receptor trafficking by secreted protein factors.Frontiers in cellular neuroscience · 2023Review
- BDNF Therapeutic Mechanisms in Neuropsychiatric Disorders.International journal of molecular sciences · 2022Review
- Cellular Effects of Rhynchophylline and Relevance to Sleep Regulation.Clocks & sleep · 2021Review
- Secreted Amyloid Precursor Protein-Alpha Enhances LTP Through the Synthesis and Trafficking of CaFrontiers in molecular neuroscience · 2021Article
- The Role of Glutamate in Language and Language Disorders - Evidence from ERP and Pharmacologic Studies.Neuroscience and biobehavioral reviews · 2020Review
- The Role of Altered BDNF/TrkB Signaling in Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2019Review
- Inhibition of the tyrosine phosphatase STEP61 restores BDNF expression and reverses motor and cognitive deficits in phencyclidine-treated mice.Cellular and molecular life sciences : CMLS · 2016Article
- Down-regulation of BDNF in cell and animal models increases striatal-enriched protein tyrosine phosphatase 61 (STEP61 ) levels.Journal of neurochemistry · 2016Article
- Coincidence detection in a neural correlate of classical conditioning is initiated by bidirectional 3-phosphoinositide-dependent kinase-1 signalling and modulated by adenosine receptors.The Journal of physiology · 2015Article
- Multiple faces of BDNF in cocaine addiction.Behavioural brain research · 2015Review
- Long-term potentiation can be induced in the CA1 region of hippocampus in the absence of αCaMKII T286-autophosphorylation.Learning & memory (Cold Spring Harbor, N.Y.) · 2014Article
- Sequential delivery of synaptic GluA1- and GluA4-containing AMPA receptors (AMPARs) by SAP97 anchored protein complexes in classical conditioning.The Journal of biological chemistry · 2014Article
- BDNF contributes to both rapid and homeostatic alterations in AMPA receptor surface expression in nucleus accumbens medium spiny neurons.The European journal of neuroscience · 2014Article
- A role for hippocampal PSA-NCAM and NMDA-NR2B receptor function in flavonoid-induced spatial memory improvements in young rats.Neuropharmacology · 2014Article
- Adaptations in AMPA receptor transmission in the nucleus accumbens contributing to incubation of cocaine craving.Neuropharmacology · 2014Review
- Different roles of BDNF in nucleus accumbens core versus shell during the incubation of cue-induced cocaine craving and its long-term maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Feedback mechanism in depolarization-induced sustained activation of extracellular signal-regulated kinase in the hippocampus.Scientific reports · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies using an in vitro model of eyeblink classical conditioning in turtles suggest that increased numbers of synaptic AMPARs supports the acquisition and expression of conditioned responses (CRs). Brain-derived neurotrophic factor (BDNF) and its associated receptor tyrosine kinase, TrkB, is also required for acquisition of CRs. Bath application of BDNF alone induces synaptic delivery of GluR1- and GluR4-containing AMPARs that is blocked by coapplication of the receptor tyrosine kinase inhibitor K252a. The molecular mechanisms involved in BDNF-induced AMPAR trafficking remain largely unknown. The aim of this study was to determine whether BDNF-induced synaptic AMPAR incorporation utilizes similar cellular mechanisms as AMPAR trafficking that occurs during in vitro classical conditioning. Using pharmacological blockade and confocal imaging, the results show that synaptic delivery of GluR1 subunits during conditioning or BDNF application does not require activity of NMDARs but is mediated by extracellular signal-regulated kinase (ERK). In contrast, synaptic delivery of GluR4-containing AMPARs during both conditioning and BDNF application is NMDAR- as well as ERK-dependent. These findings indicate that BDNF application mimics AMPAR trafficking observed during conditioning by activation of some of the same intracellular signaling pathways and suggest that BDNF is a key signal transduction element in postsynaptic events that mediate conditioning.
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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.