Sodium channel activation underlies transfluthrin repellency in Aedes aegypti

Autor: Peng Xu, Feng Liu, Wilson R. Valbon, Eugênio E. Oliveira, Aijun Zhang, Youfa Jiang, Ke Dong, Felipe Andreazza, Jeffrey G. Scott, Mengli Chen, Shaoying Wu, Elizabeth Bandason, Letícia B. Smith, Dingxin Jiang, Qiang Wang
Jazyk: angličtina
Rok vydání: 2021
Předmět:
Cyclopropanes
Insecticides
Physiology
Sodium channel gene
RC955-962
Pharmacology
Disease Vectors
Mosquitoes
Biochemistry
Sodium Channels
Ion Channels
DEET
Isomers
chemistry.chemical_compound
0302 clinical medicine
Human disease
Medical Conditions
Aedes
Stereochemistry
Arctic medicine. Tropical medicine
Principal mechanism
Medicine and Health Sciences
Materials
0303 health sciences
Pyrethroid
biology
Physics
Eukaryota
Agriculture
Insects
Electrophysiology
Chemistry
Infectious Diseases
Physical Sciences
Insect Proteins
Public aspects of medicine
RA1-1270
Agrochemicals
Research Article
animal structures
Arthropoda
030231 tropical medicine
Materials Science
Biophysics
Neurophysiology
Aedes aegypti
03 medical and health sciences
Isomerism
Animals
030304 developmental biology
Sodium channel
fungi
Public Health
Environmental and Occupational Health
Organisms
Chemical Compounds
Biology and Life Sciences
Proteins
biology.organism_classification
Invertebrates
Insect Vectors
Fluorobenzenes
Species Interactions
chemistry
Transfluthrin
Insect Repellents
Odorants
Zoology
Entomology
Neuroscience
Zdroj: PLoS Neglected Tropical Diseases, Vol 15, Iss 7, p e0009546 (2021)
PLoS Neglected Tropical Diseases
ISSN: 1935-2735
1935-2727
Popis: Background Volatile pyrethroid insecticides, such as transfluthrin, have received increasing attention for their potent repellent activities in recent years for controlling human disease vectors. It has been long understood that pyrethroids kill insects by promoting activation and inhibiting inactivation of voltage-gated sodium channels. However, the mechanism of pyrethroid repellency remains poorly understood and controversial. Methodology/Principal findings Here, we show that transfluthrin repels Aedes aegypti in a hand-in-cage assay at nonlethal concentrations as low as 1 ppm. Contrary to a previous report, transfluthrin does not elicit any electroantennogram (EAG) responses, indicating that it does not activate olfactory receptor neurons (ORNs). The 1S-cis isomer of transfluthrin, which does not activate sodium channels, does not elicit repellency. Mutations in the sodium channel gene that reduce the potency of transfluthrin on sodium channels decrease transfluthrin repellency but do not affect repellency by DEET. Furthermore, transfluthrin enhances DEET repellency. Conclusions/Significance These results provide a surprising example that sodium channel activation alone is sufficient to potently repel mosquitoes. Our findings of sodium channel activation as the principal mechanism of transfluthrin repellency and potentiation of DEET repellency have broad implications in future development of a new generation of dual-target repellent formulations to more effectively repel a variety of human disease vectors.
Author summary Vector-transmitted human diseases, such as dengue fever, represent serious global health burdens. Pyrethroids, including transfluthrin, are widely used as insecticides and repellents due to their low mammalian toxicity and relatively benign environmental impact. Pyrethroids target voltage-gated sodium channels for their insecticidal action. However, the mechanism of pyrethroid repellency remains unclear and controversial. Insect repellency is traditionally thought to be mediated by olfactory receptors. We made two important discoveries in this study, showing that transfluthrin repellency is via activation of sodium channels and transfluthrin enhances DEET repellency. Discovery of sodium channel activation as a major mechanism of pyrethroid repellency has broad significance in insect olfaction study, repellents development, and control of human disease vectors.
Databáze: OpenAIRE
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