Next Article in Journal
The Identification of a SIRT6 Activator from Brown Algae Fucus distichus
Next Article in Special Issue
Urinary Excretion of Tetrodotoxin Modeled in a Porcine Renal Proximal Tubule Epithelial Cell Line, LLC-PK1
Previous Article in Journal
The Sea Urchin Arbacia lixula: A Novel Natural Source of Astaxanthin
Previous Article in Special Issue
A Study of 11-[3H]-Tetrodotoxin Absorption, Distribution, Metabolism and Excretion (ADME) in Adult Sprague-Dawley Rats
Article

Effects of Tetrodotoxin in Mouse Models of Visceral Pain

1
Department of Pharmacology, Biomedical Research Centre and Institute of Neuroscience, Faculty of Medicine, University of Granada, 18016 Granada, Spain
2
Biosanitary Research Institute, University Hospital Complex of Granada, 18012 Granada, Spain
3
Animal Behavior Research Unit, Scientific Instrumentation Center, University of Granada, Armilla, 18100 Granada, Spain
4
Molecular Nociception Group, Wolfson Institute for Biomedical Research, University College London, London WC1E 6BT, UK
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Mar. Drugs 2017, 15(6), 188; https://doi.org/10.3390/md15060188
Received: 5 April 2017 / Revised: 7 June 2017 / Accepted: 16 June 2017 / Published: 21 June 2017
(This article belongs to the Special Issue Tetrodotoxin)
Visceral pain is very common and represents a major unmet clinical need for which current pharmacological treatments are often insufficient. Tetrodotoxin (TTX) is a potent neurotoxin that exerts analgesic actions in both humans and rodents under different somatic pain conditions, but its effect has been unexplored in visceral pain. Therefore, we tested the effects of systemic TTX in viscero-specific mouse models of chemical stimulation of the colon (intracolonic instillation of capsaicin and mustard oil) and intraperitoneal cyclophosphamide-induced cystitis. The subcutaneous administration of TTX dose-dependently inhibited the number of pain-related behaviors in all evaluated pain models and reversed the referred mechanical hyperalgesia (examined by stimulation of the abdomen with von Frey filaments) induced by capsaicin and cyclophosphamide, but not that induced by mustard oil. Morphine inhibited both pain responses and the referred mechanical hyperalgesia in all tests. Conditional nociceptor‑specific Nav1.7 knockout mice treated with TTX showed the same responses as littermate controls after the administration of the algogens. No motor incoordination after the administration of TTX was observed. These results suggest that blockade of TTX-sensitive sodium channels, but not Nav1.7 subtype alone, by systemic administration of TTX might be a potential therapeutic strategy for the treatment of visceral pain. View Full-Text
Keywords: tetrodotoxin; visceral pain; referred mechanical hyperalgesia; TTX-sensitive voltage-gated sodium channels; Nav1.7; capsaicin; mustard oil; cyclophosphamide tetrodotoxin; visceral pain; referred mechanical hyperalgesia; TTX-sensitive voltage-gated sodium channels; Nav1.7; capsaicin; mustard oil; cyclophosphamide
Show Figures

Figure 1

MDPI and ACS Style

González-Cano, R.; Tejada, M.Á.; Artacho-Cordón, A.; Nieto, F.R.; Entrena, J.M.; Wood, J.N.; Cendán, C.M. Effects of Tetrodotoxin in Mouse Models of Visceral Pain. Mar. Drugs 2017, 15, 188. https://doi.org/10.3390/md15060188

AMA Style

González-Cano R, Tejada MÁ, Artacho-Cordón A, Nieto FR, Entrena JM, Wood JN, Cendán CM. Effects of Tetrodotoxin in Mouse Models of Visceral Pain. Marine Drugs. 2017; 15(6):188. https://doi.org/10.3390/md15060188

Chicago/Turabian Style

González-Cano, Rafael, Miguel Á. Tejada, Antonia Artacho-Cordón, Francisco R. Nieto, José M. Entrena, John N. Wood, and Cruz M. Cendán 2017. "Effects of Tetrodotoxin in Mouse Models of Visceral Pain" Marine Drugs 15, no. 6: 188. https://doi.org/10.3390/md15060188

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop