ArticleThe European journal of neuroscience2014
BDNF released during neuropathic pain potentiates NMDA receptors in primary afferent terminals.
Article in The European journal of neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 102 citations in OpenAlex.
- BDNF-TrkB Signaling Engages a Src Family Kinase-Pannexin 1 Pathway During the Onset of Sustained Mechanical Hyperalgesia.International journal of molecular sciences · 2026Article
- Neuroplasticity-Driven Mechanisms and Therapeutic Targets in the Anterior Cingulate Cortex in Neuropathic Pain.Brain and behavior · 2026Review
- Neuroimmune regulation of visceral pain: roles of microglia, purinergic signaling, and neuroinflammation.Frontiers in immunology · 2026Review
- Cortical Potentiation in Chronic Neuropathic Pain and the Future Treatment.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Brain-derived neurotrophic factor contributes to activity-induced muscle pain in male but not female mice.Brain, behavior, and immunity · 2024Article
- Satellite Glial Cells Bridge Sensory Neuron Crosstalk in Visceral Pain and Cross-Organ Sensitization.The Journal of pharmacology and experimental therapeutics · 2024Review
- Indole-3-Carbinol and Its Derivatives as Neuroprotective Modulators.Brain sciences · 2024Review
- Brain-Derived Neurotrophic Factor, Nociception, and Pain.Biomolecules · 2024Review
- Brain-derived neurotrophic factor contributes to activity-induced muscle pain in male but not female mice.bioRxiv : the preprint server for biology · 2023Article
- Neurotrophin-3 (NT-3) as a Potential Biomarker of the Peripheral Nervous System Damage Following Breast Cancer Treatment.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Article
- BDNF as a biomarker for neuropathic pain: Consideration of mechanisms of action and associated measurement challenges.Brain and behavior · 2023Review
- Effect of Different Physical Therapy Interventions on Brain-Derived Neurotrophic Factor Levels in Chronic Musculoskeletal Pain Patients: A Systematic Review.Life (Basel, Switzerland) · 2023Review
- Neuropathic pain; what we know and what we should do about it.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Article
- Presynaptic NMDARs on spinal nociceptor terminals state-dependently modulate synaptic transmission and pain.Nature communications · 2022Article
- Advances and Barriers in Understanding PresynapticFrontiers in molecular neuroscience · 2022Review
- Shedding Light on the Pharmacological Interactions between μ-Opioid Analgesics and Angiotensin Receptor Modulators: A New Option for Treating Chronic Pain.Molecules (Basel, Switzerland) · 2021Review
- Article
- cAMP signaling through protein kinase A and Epac2 induces substance P release in the rat spinal cord.Neuropharmacology · 2021Article
- Microglia and Inhibitory Circuitry in the Medullary Dorsal Horn: Laminar and Time-Dependent Changes in a Trigeminal Model of Neuropathic Pain.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
NMDA receptors in primary afferent terminals can contribute to hyperalgesia by increasing neurotransmitter release. In rats and mice, we found that the ability of intrathecal NMDA to induce neurokinin 1 receptor (NK1R) internalization (a measure of substance P release) required a previous injection of BDNF. Selective knock-down of NMDA receptors in primary afferents decreased NMDA-induced NK1R internalization, confirming the presynaptic location of these receptors. The effect of BDNF was mediated by tropomyosin-related kinase B (trkB) receptors and not p75 neurotrophin receptors (p75(NTR) ), because it was not produced by proBDNF and was inhibited by the trkB antagonist ANA-12 but not by the p75(NTR) inhibitor TAT-Pep5. These effects are probably mediated through the truncated form of the trkB receptor as there is little expression of full-length trkB in dorsal root ganglion (DRG) neurons. Src family kinase inhibitors blocked the effect of BDNF, suggesting that trkB receptors promote the activation of these NMDA receptors by Src family kinase phosphorylation. Western blots of cultured DRG neurons revealed that BDNF increased Tyr(1472) phosphorylation of the NR2B subunit of the NMDA receptor, known to have a potentiating effect. Patch-clamp recordings showed that BDNF, but not proBDNF, increased NMDA receptor currents in cultured DRG neurons. NMDA-induced NK1R internalization was also enabled in a neuropathic pain model or by activating dorsal horn microglia with lipopolysaccharide. These effects were decreased by a BDNF scavenger, a trkB receptor antagonist and a Src family kinase inhibitor, indicating that BDNF released by microglia potentiates NMDA receptors in primary afferents during neuropathic pain.
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