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.
Lionfish venom causes extreme pain through unknown mechanisms. Here, we characterize the pain this venom produces and demonstrate it predominantly targets nonpeptidergic nociceptors.
aDepartment of Physiology and Cell Information Systems, McGill University, Montreal, QC, Canada
bNeurosciences and Mental Health, The Hospital for Sick Children, Toronto, ON, Canada
cDepartment of Physiology and Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, ON, Canada
dAlan Edwards Center for Research in Pain, McGill University, Montreal, QC, Canada
Corresponding author. Address: Department of Physiology & Cell Information Systems Group, McGill University, Life Sciences Complex (Bellini), Suite 171, 3649 Promenade Sir William Osler, Montréal, Québec H3G 0B1. Tel.: 514-398-5361. E-mail address: Reza.email@example.com (R. Sharif-Naeini).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Received October 24, 2017
Received in revised form June 11, 2018
Accepted June 25, 2018