ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
TrkB.T1 contributes to neuropathic pain after spinal cord injury through regulation of cell cycle pathways.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- TrkB Truncated Isoform Receptors as Transducers and Determinants of BDNF Functions.Frontiers in neuroscience · 2022Pooled it
- Integrative bulk and single-cell transcriptome analyses reveal RNA modification-related biomarkers of spinal cord injury.Neural regeneration research · 2026Article
- Machine learning identifies key cells and therapeutic targets during ferroptosis after spinal cord injury.Neural regeneration research · 2026Article
- Integrative single-cell and bulk transcriptomic analyses identify a microglia-associated NAGLU signature linked to disulfidptosis-associated transcriptional patterns after spinal cord injury.Frontiers in immunology · 2026Article
- Multi-omics identifies a VIM-associated microglial program linked to lactylation, ferroptosis, and neuroinflammation after spinal cord injury.Frontiers in genetics · 2026Article
- Role of astrocytes in diabetic neuropathy: Review of their involvement in disease mechanisms.World journal of diabetes · 2025Review
- Truncated TrkB: The predominant TrkB isoform in nociceptors.The journal of pain · 2025Article
- Metabolic Reprogramming in Spinal Cord Injury and Analysis of Potential Therapeutic Targets.Journal of molecular neuroscience : MN · 2025Article
- BDNF-TrkB Signaling Pathway in Spinal Cord Injury: Insights and Implications.Molecular neurobiology · 2025Review
- Article
- Exploring hypoxia-related genes in spinal cord injury: a pathway to new therapeutic targets.Frontiers in molecular neuroscience · 2025Article
- Article
- Genetic Variations in TrkB.T1 Isoform and Their Association With Somatic and Psychological Symptoms in Individuals With IBS.The journal of pain · 2024Article
- Satellite Glial Cells Bridge Sensory Neuron Crosstalk in Visceral Pain and Cross-Organ Sensitization.The Journal of pharmacology and experimental therapeutics · 2024Review
- Brain-Derived Neurotrophic Factor, Nociception, and Pain.Biomolecules · 2024Review
- Article
- Long noncoding RNA small nucleolar RNA host gene 5 facilitates neuropathic pain in spinal nerve injury by promoting SCN9A expression via CDK9.Human cell · 2024Article
- Omega-conotoxin MVIIA reduces neuropathic pain after spinal cord injury by inhibiting N-type voltage-dependent calcium channels on spinal dorsal horn.Frontiers in neuroscience · 2024Article
- Intrathecal dexmedetomidine attenuates mechanical allodynia through the downregulation of brain-derived neurotrophic factor in a mild traumatic brain injury rat model.Korean journal of anesthesiology · 2023Article
- Transient Reflexive Pain Responses and Chronic Affective Nonreflexive Pain Responses Associated with Neuroinflammation Processes in Both Spinal and Supraspinal Structures in Spinal Cord-Injured Female Mice.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Spinal cord injury (SCI) frequently causes severe, persistent central neuropathic pain that responds poorly to conventional pain treatments. Brain-derived neurotrophic factor (BDNF) signaling appears to contribute to central sensitization and nocifensive behaviors in certain animal models of chronic pain through effects mediated in part by the alternatively spliced truncated isoform of the BDNF receptor tropomyosin-related kinase B.T1 (trkB.T1). Mechanisms linking trkB.T1 to SCI-induced chronic central pain are unknown. Here, we examined the role of trkB.T1 in central neuropathic pain after spinal cord contusion. Genetic deletion of trkB.T1 in mice significantly reduced post-SCI mechanical hyperesthesia, locomotor dysfunction, lesion volumes, and white matter loss. Whole genome analysis, confirmed at the protein level, revealed that cell cycle genes were upregulated in trkB.T1(+/+) but not trkB.T1(-/-) spinal cord after SCI. TGFβ-induced reactive astrocytes from WT mice showed increased cell cycle protein expression that was significantly reduced in astrocytes from trkB.T1(-/-) mice that express neither full-length trkB nor trkB.T1. Administration of CR8, which selectively inhibits cyclin-dependent kinases, reduced hyperesthesia, locomotor deficits, and dorsal horn (SDH) glial changes after SCI, similar to trkB.T1 deletion, without altering trkB.T1 protein expression. In trkB.T1(-/-) mice, CR8 had no effect. These data indicate that trkB.T1 contributes to the pathobiology of SCI and SCI pain through modulation of cell cycle pathways and suggest new therapeutic targets.
Indexed as
Identifiers
What OpenQuestion holds
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.