ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Reduced nerve injury-induced neuropathic pain in kinin B1 receptor knock-out mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. 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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Who cites it
23 citing papers in PubMed, 87 citations in OpenAlex.
- Bradykinin receptor expression and bradykinin-mediated sensitization of human sensory neurons.bioRxiv : the preprint server for biology · 2023Article
- Comparative neuroprotective effects of Cerebrolysin, dexamethasone, and ascorbic acid on sciatic nerve injury model: Behavioral and histopathological study.Frontiers in neuroanatomy · 2023Article
- A compendium of validated pain genes.WIREs mechanisms of disease · 2022Review
- Ramipril Alleviates Oxaliplatin-Induced Acute Pain Syndrome in Mice.Frontiers in pharmacology · 2021Article
- Reciprocal Regulatory Interaction between TRPV1 and Kinin B1 Receptor in a Rat Neuropathic Pain Model.International journal of molecular sciences · 2020Article
- Mechanisms for Reducing Neuropathic Pain.Molecular neurobiology · 2020Review
- Depolarizing Effectors of Bradykinin Signaling in Nociceptor Excitation in Pain Perception.Biomolecules & therapeutics · 2018Review
- Potentiation of Paclitaxel-Induced Pain Syndrome in Mice by Angiotensin I Converting Enzyme Inhibition and Involvement of Kinins.Molecular neurobiology · 2017Article
- Anti-nociceptive effect of stigmasterol in mouse models of acute and chronic pain.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Antinociceptive Activities of the Methanolic Extract of the Stem Bark ofEvidence-based complementary and alternative medicine : eCAM · 2017Article
- Food-Derived Natural Compounds for Pain Relief in Neuropathic Pain.BioMed research international · 2016Review
- Spinal cord injury induced neuropathic pain: Molecular targets and therapeutic approaches.Metabolic brain disease · 2015Review
- Effects of kinin B(1) and B(2) receptor antagonists on overactive urinary bladder syndrome induced by spinal cord injury in rats.British journal of pharmacology · 2012Article
- Neuropathic pain: role of inflammation, immune response, and ion channel activity in central injury mechanisms.Annals of neurosciences · 2012Review
- PKCε phosphorylation of the sodium channel NaV1.8 increases channel function and produces mechanical hyperalgesia in mice.The Journal of clinical investigation · 2012Article
- Anti-nociceptive effect of kinin B₁ and B₂ receptor antagonists on peripheral neuropathy induced by paclitaxel in mice.British journal of pharmacology · 2011Article
- Some new insights into the molecular mechanisms of pain perception.The Journal of clinical investigation · 2010Article
- Neuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B1 and B2 receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- A novel inflammatory pathway involved in leukocyte recruitment: role for the kinin B1 receptor and the chemokine CXCL5.Journal of immunology (Baltimore, Md. : 1950) · 2007Article
- The kinin B1 receptor antagonist SSR240612 reverses tactile and cold allodynia in an experimental rat model of insulin resistance.British journal of pharmacology · 2007Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Injury to peripheral nerves often results in a persistent neuropathic pain condition that is characterized by spontaneous pain, allodynia, and hyperalgesia. Nerve injury is accompanied by a local inflammatory reaction in which nerve-associated and immune cells release several pronociceptive mediators. Kinin B1 receptors are rarely expressed in nontraumatized tissues, but they can be expressed after tissue injury. Because B1 receptors mediate chronic inflammatory painful processes, we studied their participation in neuropathic pain using receptor gene-deleted mice. In the absence of neuropathy, we found no difference in the paw-withdrawal responses to thermal or mechanical stimulation between B1 receptor knock-out mice and 129/J wild-type mice. Partial ligation of the sciatic nerve in the wild-type mouse produced a profound and long-lasting decrease in thermal and mechanical thresholds in the paw ipsilateral to nerve lesion. Threshold changed neither in the sham-operated animals nor in the paw contralateral to lesion. Ablation of the gene for the B1 receptor resulted in a significant reduction in early stages of mechanical allodynia and thermal hyperalgesia. Furthermore, systemic treatment with the B1 selective receptor antagonist des-Arg9-[Leu8]-bradykinin reduced the established mechanical allodynia observed 7-28 d after nerve lesion in wild-type mice. Partial sciatic nerve ligation induced an upregulation in B1 receptor mRNA in ipsilateral paw, sciatic nerve, and spinal cord of wild-type mice. Together, kinin B1 receptor activation seems to be essential to neuropathic pain development, suggesting that an oral-selective B1 receptor antagonist might have therapeutic potential in the management of chronic pain.
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