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 |
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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 |
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