ArticleMolecular pain2008
Targeted mutation of EphB1 receptor prevents development of neuropathic hyperalgesia and physical dependence on morphine in mice.
Article in Molecular pain, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- Blockade of Erythropoietin-Producing Human Hepatocellular Carcinoma Receptor B1 in Spinal Dorsal Horn Alleviates Visceral Pain in Rats.Pain research & management · 2021Trial
- EphB1 Receptor Blockade Augments Morphine Antinociception via Inhibiting GRK2-Mediated µ-Opioid Receptor Internalization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- EphB1-NR2B receptor signaling in glutamatergic neurons of the ventroposteromedial thalamic nucleus regulates emergence from anesthesia.Science advances · 2025Article
- Discovery of pan-EphB tyrosine kinase inhibitor for metabolic syndrome sparing EphB3 signaling in mice.Pharmacological research · 2025Article
- Genomic evidence for behavioral adaptation of herding dogs.Science advances · 2025Article
- ephrin-B2 promotes nociceptive plasticity and hyperalgesic priming through EphB2-MNK-eIF4E signaling in both mice and humans.Pharmacological research · 2024Article
- Multi-animal-model study reveals mutations in neural plasticity and nociception genes linked to excessive alcohol drinking.Alcohol, clinical & experimental research · 2023Article
- Mu-opioid receptor and receptor tyrosine kinase crosstalk: Implications in mechanisms of opioid tolerance, reduced analgesia to neuropathic pain, dependence, and reward.Frontiers in systems neuroscience · 2022Review
- Identification of tetracycline combinations as EphB1 tyrosine kinase inhibitors for treatment of neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- EphB2 receptor cell-autonomous forward signaling mediates auditory memory recall and learning-driven spinogenesis.Communications biology · 2019Article
- EphBs and ephrin-Bs: Trans-synaptic organizers of synapse development and function.Molecular and cellular neurosciences · 2018Review
- Extracellular phosphorylation of a receptor tyrosine kinase controls synaptic localization of NMDA receptors and regulates pathological pain.PLoS biology · 2017Article
- The Role of Ephs and Ephrins in Memory Formation.The international journal of neuropsychopharmacology · 2016Review
- Knockdown of EphB1 receptor decreases medulloblastoma cell growth and migration and increases cellular radiosensitization.Oncotarget · 2015Article
- Ephrin-B2 expression in the proprioceptive sensory system.Neuroscience letters · 2013Article
- WNT signaling underlies the pathogenesis of neuropathic pain in rodents.The Journal of clinical investigation · 2013Article
- Involvement of EphB1 receptors signalling in models of inflammatory and neuropathic pain.PloS one · 2013Article
- EphBs: an integral link between synaptic function and synaptopathies.Trends in neurosciences · 2012Review
- Nociceptor-expressed ephrin-B2 regulates inflammatory and neuropathic pain.Molecular pain · 2010Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
EphB receptor tyrosine kinases, which play important roles in synaptic connection and plasticity during development and in matured nervous system, have recently been implicated in processing of pain after nerve injury and morphine dependence. Subtypes of the EphB receptors that may contribute to the neuropathic pain and morphine dependence have not been identified. Here we demonstrate that the subtype EphB1 receptor is necessary for development of neuropathic pain and physical dependence on morphine. The results showed that peripheral nerve injury produced thermal hyperalgesia in wild-type (EphB1+/+) control littermate mice, but not in EphB1 receptor homozygous knockout (EphB1-/-) and heterozygous knockdown (EphB1+/-) mice. Hyperalgesia in the wild-type mice was inhibited by intrathecal administration of an EphB receptor blocking reagent EphB2-Fc (2 microg). Intrathecal administration of an EphB receptor activator ephrinB1-Fc (1 microg) evoked thermal hyperalgesia in EphB1+/+, but not EphB1-/- and EphB1+/- mice. Cellularly, nerve injury-induced hyperexcitability of the medium-sized dorsal root ganglion neurons was prevented in EphB1-/- and EphB1+/- mice. In chronically morphine-treated mice, most of the behavioral signs and the overall score of naloxone-precipitated withdrawal were largely diminished in EphB1-/- mice compared to those in the wild-type. These findings indicate that the EphB1 receptor is necessary for development of neuropathic pain and physical dependence on morphine and suggest that the EphB1 receptor is a potential target for preventing, minimizing, or reversing the development of neuropathic pain and opiate dependence.
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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.