Lionfish venom elicits pain predominantly through the activation of nonpeptidergic nociceptors

Autor: Steven A. Prescott, Reza Sharif-Naeini, Stephanie Mouchbahani-Constance, Albena Davidova, Hugues Petitjean, L. Stephen Lesperance, Amanda MacPherson
Rok vydání: 2018
Předmět:
0301 basic medicine
Time Factors
Poison control
Venom
Pharmacology
Mice
0302 clinical medicine
Fish Venoms
Ganglia
Spinal

Medicine
Pain Measurement
Neurogenic inflammation
Microglia
Microfilament Proteins
medicine.anatomical_structure
Neurology
Hyperalgesia
Nociceptor
Neurogenic Inflammation
medicine.symptom
Sensory Receptor Cells
Green Fluorescent Proteins
Pain
TRPV Cation Channels
Mice
Transgenic

Inflammation
03 medical and health sciences
Calcium imaging
Animals
Humans
Envenomation
Acrylamides
Analysis of Variance
Dose-Response Relationship
Drug

business.industry
Calcium-Binding Proteins
Bridged Bicyclo Compounds
Heterocyclic

Mice
Inbred C57BL

Disease Models
Animal

Luminescent Proteins
HEK293 Cells
Oncogene Proteins v-fos
030104 developmental biology
Anesthesiology and Pain Medicine
Gene Expression Regulation
Touch
Exploratory Behavior
Calcium
Neurology (clinical)
Capsaicin
business
030217 neurology & neurosurgery
Zdroj: Pain. 159:2255-2266
ISSN: 1872-6623
0304-3959
Popis: The lionfish (Pterois volitans) is a venomous invasive species found in the Caribbean and Northwestern Atlantic. It poses a growing health problem because of the increase in frequency of painful stings, for which no treatment or antidote exists, and the long-term disability caused by the pain. Understanding the venom's algogenic properties can help identify better treatment for these envenomations. In this study, we provide the first characterization of the pain and inflammation caused by lionfish venom and examine the mechanisms through which it causes pain using a combination of in vivo and in vitro approaches including behavioral, physiological, calcium imaging, and electrophysiological testing. Intraplantar injections of the venom produce a significant increase in pain behavior, as well as a marked increase in mechanical sensitivity for up to 24 hours after injection. The algogenic substance(s) are heat-labile peptides that cause neurogenic inflammation at the site of injection and induction of Fos and microglia activation in the superficial layers of the dorsal horn. Finally, calcium imaging and electrophysiology experiments show that the venom acts predominantly on nonpeptidergic, TRPV1-negative, nociceptors, a subset of neurons implicated in sensing mechanical pain. These data provide the first characterization of the pain and inflammation caused by lionfish venom, as well as the first insight into its possible cellular mechanism of action.
Databáze: OpenAIRE