Tags

Type your tag names separated by a space and hit enter

Peripheral kinin B(1) and B(2) receptor-operated mechanisms are implicated in neuropathic nociception induced by spinal nerve ligation in rats.
Neuropharmacology. 2007 Jul; 53(1):48-57.N

Abstract

The kinin system can contribute distinctly to the sensory changes associated with different models of nerve injury-induced neuropathic pain. This study examines the roles of kinin B(1) and B(2) receptor-operated mechanisms in alterations in nociceptive responses of rats submitted to unilateral L5/L6 spinal nerve ligation (SNL) injury. Behavioural responses to ipsilateral hind paw stimulation with acetone (evaporation-evoked cooling), radiant heat (Hargreaves method) or von Frey hairs revealed that SNL rats developed long-lasting cold allodynia (from Days 3 to 40 post-surgery, peak on Day 6), heat hyperalgesia (stable peak from Days 9 to 36) and tactile allodynia (stable peak from Days 3 to 51). SNL rats manifested nocifensive responses to intraplantar injections on Day 12 of the selective B(1) receptor agonist des-Arg(9)-bradykinin (DABK) and augmented responses to the selective B(2) receptor agonist bradykinin (BK; each at 0.01-1nmol/paw). Systemic treatment of SNL rats with des-Arg(9)-Leu(8)-BK or HOE 140 (peptidic B(1) and B(2) receptor antagonists, respectively; 0.1-1mumol/kg, i.p.) selectively blocked responses triggered by DABK and BK (1nmol/paw) and alleviated partially and transiently established cold allodynia, heat hyperalgesia and (to a lesser extent) tactile allodynia. Western blot analysis revealed enhanced expression of kinin B(1) and B(2) receptor protein in ipsilateral L4-L6 spinal nerve and hind paw skin samples collected on Day 12 after SNL surgery. These results indicate that peripheral pronociceptive kinin B(1) and B(2) receptor-operated mechanisms contribute significantly to the maintenance of hind paw cold and mechanical allodynia and heat hyperalgesia induced by L5/L6 SNL in rats.

Authors+Show Affiliations

Department of Pharmacology, Biological Sciences Center, Universidade Federal de Santa Catarina, Florianópolis, 88048-900 SC, Brazil.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17555775

Citation

Werner, M F P., et al. "Peripheral Kinin B(1) and B(2) Receptor-operated Mechanisms Are Implicated in Neuropathic Nociception Induced By Spinal Nerve Ligation in Rats." Neuropharmacology, vol. 53, no. 1, 2007, pp. 48-57.
Werner MF, Kassuya CA, Ferreira J, et al. Peripheral kinin B(1) and B(2) receptor-operated mechanisms are implicated in neuropathic nociception induced by spinal nerve ligation in rats. Neuropharmacology. 2007;53(1):48-57.
Werner, M. F., Kassuya, C. A., Ferreira, J., Zampronio, A. R., Calixto, J. B., & Rae, G. A. (2007). Peripheral kinin B(1) and B(2) receptor-operated mechanisms are implicated in neuropathic nociception induced by spinal nerve ligation in rats. Neuropharmacology, 53(1), 48-57.
Werner MF, et al. Peripheral Kinin B(1) and B(2) Receptor-operated Mechanisms Are Implicated in Neuropathic Nociception Induced By Spinal Nerve Ligation in Rats. Neuropharmacology. 2007;53(1):48-57. PubMed PMID: 17555775.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Peripheral kinin B(1) and B(2) receptor-operated mechanisms are implicated in neuropathic nociception induced by spinal nerve ligation in rats. AU - Werner,M F P, AU - Kassuya,C A L, AU - Ferreira,J, AU - Zampronio,A R, AU - Calixto,J B, AU - Rae,G A, Y1 - 2007/05/03/ PY - 2007/01/25/received PY - 2007/03/30/revised PY - 2007/04/12/accepted PY - 2007/6/9/pubmed PY - 2007/11/10/medline PY - 2007/6/9/entrez SP - 48 EP - 57 JF - Neuropharmacology JO - Neuropharmacology VL - 53 IS - 1 N2 - The kinin system can contribute distinctly to the sensory changes associated with different models of nerve injury-induced neuropathic pain. This study examines the roles of kinin B(1) and B(2) receptor-operated mechanisms in alterations in nociceptive responses of rats submitted to unilateral L5/L6 spinal nerve ligation (SNL) injury. Behavioural responses to ipsilateral hind paw stimulation with acetone (evaporation-evoked cooling), radiant heat (Hargreaves method) or von Frey hairs revealed that SNL rats developed long-lasting cold allodynia (from Days 3 to 40 post-surgery, peak on Day 6), heat hyperalgesia (stable peak from Days 9 to 36) and tactile allodynia (stable peak from Days 3 to 51). SNL rats manifested nocifensive responses to intraplantar injections on Day 12 of the selective B(1) receptor agonist des-Arg(9)-bradykinin (DABK) and augmented responses to the selective B(2) receptor agonist bradykinin (BK; each at 0.01-1nmol/paw). Systemic treatment of SNL rats with des-Arg(9)-Leu(8)-BK or HOE 140 (peptidic B(1) and B(2) receptor antagonists, respectively; 0.1-1mumol/kg, i.p.) selectively blocked responses triggered by DABK and BK (1nmol/paw) and alleviated partially and transiently established cold allodynia, heat hyperalgesia and (to a lesser extent) tactile allodynia. Western blot analysis revealed enhanced expression of kinin B(1) and B(2) receptor protein in ipsilateral L4-L6 spinal nerve and hind paw skin samples collected on Day 12 after SNL surgery. These results indicate that peripheral pronociceptive kinin B(1) and B(2) receptor-operated mechanisms contribute significantly to the maintenance of hind paw cold and mechanical allodynia and heat hyperalgesia induced by L5/L6 SNL in rats. SN - 0028-3908 UR - https://www.unboundmedicine.com/medline/citation/17555775/Peripheral_kinin_B_1__and_B_2__receptor_operated_mechanisms_are_implicated_in_neuropathic_nociception_induced_by_spinal_nerve_ligation_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(07)00109-8 DB - PRIME DP - Unbound Medicine ER -