ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Neuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B1 and B2 receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 54 citations in OpenAlex.
- The Burning Pain Transcriptome in the Mouse Primary Somatosensory Cortex.International journal of molecular sciences · 2025Article
- Deletion of kinin receptor B2 enhances orthodontic tooth movement and alveolar bone remodeling.PloS one · 2025Article
- Kinin BPharmaceutics · 2023Article
- Bradykinin Receptors Play a Critical Role in the Chronic Post-ischaemia Pain Model.Cellular and molecular neurobiology · 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
- Comparison of Different In Vivo Animal Models of Brachial Plexus Avulsion and Its Application in Pain Study.Neural plasticity · 2020Review
- The kinin BInflammopharmacology · 2019Article
- Renal and vascular effects of kallikrein inhibition in a model of Lonomia obliqua venom-induced acute kidney injury.PLoS neglected tropical diseases · 2019Article
- Beneficial Effects of the Calcium Channel Blocker CTK 01512-2 in a Mouse Model of Multiple Sclerosis.Molecular neurobiology · 2018Article
- 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
- Primary Role for Kinin BMolecular neurobiology · 2017Article
- GRPR/PI3Kγ: Partners in Central Transmission of Itch.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Spinal blockage of P/Q- or N-type voltage-gated calcium channels modulates functional and symptomatic changes related to haemorrhagic cystitis in mice.British journal of pharmacology · 2015Article
- Inflammatory muscle pain is dependent on the activation of kinin B₁ and B₂ receptors and intracellular kinase pathways.British journal of pharmacology · 2012Article
- Anti-nociceptive effect of kinin B₁ and B₂ receptor antagonists on peripheral neuropathy induced by paclitaxel in mice.British journal of pharmacology · 2011Article
- Cannabinoid agonists inhibit neuropathic pain induced by brachial plexus avulsion in mice by affecting glial cells and MAP kinases.PloS one · 2011Article
- Kinin B1 receptors mediate depression-like behavior response in stressed mice treated with systemic E. coli lipopolysaccharide.Journal of neuroinflammation · 2010Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The relevance of kinin B(1) (B(1)R) and B(2) (B(2)R) receptors in the brachial plexus avulsion (BPA) model was evaluated in mice, by means of genetic and pharmacological tools. BPA-induced hypernociception was absent in B(1)R, but not in B(2)R, knock-out mice. Local or intraperitoneal administration of the B(2)R antagonist Hoe 140 failed to affect BPA-induced mechanical hypernociception. Interestingly, local or intraperitoneal treatment with B(1)R antagonists, R-715 or SSR240612, dosed at the time of surgery, significantly reduced BPA-evoked mechanical hypernociception. Intrathecal or intracerebroventricular administration of these antagonists, at the surgery moment, did not prevent the hypernociception. Both antagonists, dosed by intraperitoneal or intrathecal routes (but not intracerebroventricularly) 4 d after the surgery, significantly inhibited the mechanical hypernociception. At 30 d after the BPA, only the intracerebroventricular treatment effectively reduced the hypernociception. A marked increase in B(1)R mRNA was observed in the hypothalamus, hippocampus, thalamus, and cortex at 4 d after BPA and only in the hypothalamus and cortex at 30 d. In the spinal cord, a slight increase in B(1)R mRNA expression was observed as early as at 2 d. Finally, an enhancement of B(1)R protein expression was found in all the analyzed brain structures at 4 and 30 d after the BPA, whereas in the spinal cord, this parameter was augmented only at 4 d. The data provide new evidence on the role of peripheral and central kinin B(1)R in the BPA model of neuropathic pain. Selective B(1)R antagonists might well represent valuable tools for the management of neuropathic pain.
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