ArticlePain2017
Targeting brain-derived neurotrophic factor in the medial thalamus for the treatment of central poststroke pain in a rodent model.
Article in Pain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Targeting the posterior thalamic hub: hemispheric-specific encoding of pain-depression comorbidity after hemorrhagic stroke.BMC medicine · 2026Article
- EEG neurofeedback for the treatment of neuropathic pain in the elderly-a mechanistic review.GeroScience · 2026Review
- A comprehensive review on pain: Model, target, therapy, and prospect (Review).International journal of molecular medicine · 2026Review
- Central post-stroke pain: advances in clinical and preclinical research.Stroke and vascular neurology · 2025Review
- BDNF Signaling and Pain Modulation.Cells · 2025Review
- Oxymatrine Alleviates Central Post-Stroke Pain in Rats by Reducing the Inflammatory Response.Journal of pain research · 2025Article
- Role of Brain Derived Neurotrophic Factor and Related Therapeutic Strategies in Central Post-Stroke Pain.Neurochemical research · 2024Review
- The P2X7 Hypothesis of Central Post-Stroke Pain.International journal of molecular sciences · 2024Article
- Brain-Derived Neurotrophic Factor, Nociception, and Pain.Biomolecules · 2024Review
- Research Progress on the Mechanisms of Central Post-Stroke Pain: A Review.Cellular and molecular neurobiology · 2023Review
- Stroke-Induced Central Pain: Overview of the Mechanisms, Management, and Emerging Targets of Central Post-Stroke Pain.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Spinal MCP-1 Contributes to Central Post-stroke Pain by Inducing Central Sensitization in Rats.Molecular neurobiology · 2023Article
- Stellate ganglion block ameliorated central post-stroke pain with comorbid anxiety and depression through inhibiting HIF-1α/NLRP3 signaling following thalamic hemorrhagic stroke.Journal of neuroinflammation · 2023Article
- Role of Sensory Pathway Injury in Central Post-Stroke Pain: A Narrative Review of Its Pathogenetic Mechanism.Journal of pain research · 2023Review
- Modulation of melatonin to the thalamic lesion-induced pain and comorbid sleep disturbance in the animal model of the central post-stroke hemorrhage.Molecular pain · 2022Article
- The effect and mechanism of exercise for post-stroke pain.Frontiers in molecular neuroscience · 2022Review
- Biological Mechanism on SIRT1/NLRP3/IL-18 Signaling Pathway of Acupuncture for Treatment of Ischemic Stroke with Center Poststroke Pain.Computational intelligence and neuroscience · 2022Article
- Baicalin Attenuates Oxygen-Glucose Deprivation/Reoxygenation-Induced Injury by Modulating the BDNF-TrkB/PI3K/Akt and MAPK/Erk1/2 Signaling Axes in Neuron-Astrocyte Cocultures.Frontiers in pharmacology · 2021Article
- Interplay of BDNF and GDNF in the Mature Spinal Somatosensory System and Its Potential Therapeutic Relevance.Current neuropharmacology · 2021Review
- The Neural Bases of Tinnitus: Lessons from Deafness and Cochlear Implants.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Approximately 7% to 10% of patients develop a chronic pain syndrome after stroke. This chronic pain condition is called central poststroke pain (CPSP). Recent studies have observed an abnormal increase in the secretion of brain-derived neurotrophic factor (BDNF) in spinal cord tissue after spinal cord injury. An animal model of CPSP was established by an intrathalamus injection of collagenase. Mechanical and thermal allodynia was induced after lesions of the thalamic ventral basal complex in rats. Four weeks after the injection, the number of neurons decreased, the number of astrocytes, microglia, and P2X4 receptors increased, and BDNF mRNA expression increased in the brain lesion area. Nociceptive activity in the medial thalamus (MT) and the coherence coefficient of spontaneous field potential oscillations in the anterior cingulate cortex were enhanced in CPSP animals, and these enhancements were blocked by an acute injection of TrkB-Fc and TrkB antagonist Tat Cyclotraxin-B. Instead of being inhibited by the γ-aminobutyric acid (GABA) system in normal rats, multiunit activity in the MT was enhanced after a microinjection of muscimol, a GABAA receptor agonist, in CPSP animals. After CPSP, BDNF expression was enhanced in the MT, whereas the expression of GABAA channels and the cotransporter KCC2 decreased in the same area. These findings suggest that neuronal plasticity in the MT that was induced by BDNF overexpression after the thalamic lesion was a key factor in CPSP.
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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.