Advanced search
Start date
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Potamotrygon motoro stingray venom induces both neurogenic and inflammatory pain behavior in rodents

Full text
Kimura, L. F. [1, 2] ; Santos-Neto, M. [3] ; Barbaro, K. C. [3] ; Picolo, G. [1]
Total Authors: 4
[1] Inst Butantan, Lab Especial Dor & Sinalizacao, Av Vital Brasil 1500, BR-05503900 Sao Paulo, SP - Brazil
[2] Univ Sao Paulo, Inst Ciencias Biomed 1, Dept Farmacol, Sao Paulo, SP - Brazil
[3] Inst Butantan, Lab Imunopatol, Sao Paulo, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Toxicon; v. 150, p. 168-174, AUG 2018.
Web of Science Citations: 0

Freshwater stingray accidents cause an immediate, intense, and unrelieved pain which is followed by edema, erythema and necrosis formation. Treatment for stingray envenomation is based on administration of analgesic, antipyretic and anti-inflammatory drugs. Concerning pain control, it is prescribed to immerse punctured limb on hot water to alleviate pain. There are no studies demonstrating specific targets on which stingray venom acts to promote pain. Therefore, the aim of this work was to investigate some mechanisms of Potamotrygon motoro venom (PmV) that contribute to nociception induction. Evaluating spontaneous pain behavior in mice injected with PmV, it was seen that PmV induced both neurogenic and inflammatory pain. PmV also induced hyperalgesia in both mice and rats, evaluated through electronic von Frey and rat paw pressure test, respectively. Partial inhibition of hyperalgesia was observed in mice treated with cromolyn or promethazine, which indicated that mast cell and histamine via H1 receptor participate in the inflammatory pain. To search for some targets involved in PmVinduced hyperalgesia, the participation of TRPV1, calcium channels, neurokinins, CGRP, and norepinephrine, was evaluated in rats. It was seen that PmV-induced hyperalgesia occurs with the participation of neurokinins, mainly via NK1 receptor, CGRP, and calcium influx, through both P/Q and L-type voltage dependent calcium channels, besides TRPV1 activation. The data presented herein indicate that PmV causes hyperalgesia in rodents which is dependent on the participation of several neuroinflammatory mediators. (AU)

FAPESP's process: 08/57898-0 - National Institute of Science and Technology on Toxins
Grantee:Osvaldo Augusto Brazil Esteves Sant'Anna
Support type: Research Projects - Thematic Grants
FAPESP's process: 12/00166-3 - Participation of mast cells and histamine on inflammatory events induced by Potamotrygon motoro stingray venom in murine model
Grantee:Katia Cristina Barbaro Nogueira
Support type: Regular Research Grants