Compensatory mechanisms in resistant Anopheles gambiae AcerKis and KdrKis neurons modulate insecticide-based mosquito control.

ABSTRACT: In the malaria vector Anopheles gambiae, two point mutations in the acetylcholinesterase (ace-1^R) and the sodium channel (kdr^R) genes confer resistance to organophosphate/carbamate and pyrethroid insecticides, respectively. The mechanisms of compensation that recover the functional alterations associated with these mutations and their role in the modulation of insecticide efficacy are unknown. Using multidisciplinary approaches adapted to neurons isolated from resistant Anopheles gambiae AcerKis and KdrKis strains together with larval bioassays, we demonstrate that nAChRs, and the intracellular calcium concentration represent the key components of an adaptation strategy ensuring neuronal functions maintenance. In AcerKis neurons, the increased effect of acetylcholine

SUBMITTER: Perrier S 

PROVIDER: S-EPMC8172894 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature