@article{fdi:010082276,
  title = {{C}ompensatory mechanisms in resistant {A}nopheles gambiae {A}cer{K}is and {K}dr{K}is neurons modulate insecticide-based mosquito control},
  author = {{P}errier, {S}. and {M}oreau, {E}. and {D}eshayes, {C}. and {E}l-{A}douzi, {M}. and {G}oven, {D}. and {C}handre, {F}abrice and {L}apied, {B}.},
  editor = {},
  language = {{ENG}},
  abstract = {{I}n the malaria vector {A}nopheles 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. {T}he mechanisms of compensation that recover the functional alterations associated with these mutations and their role in the modulation of insecticide efficacy are unknown. {U}sing multidisciplinary approaches adapted to neurons isolated from resistant {A}nopheles gambiae {A}cer{K}is and {K}dr{K}is strains together with larval bioassays, we demonstrate that n{AC}h{R}s, and the intracellular calcium concentration represent the key components of an adaptation strategy ensuring neuronal functions maintenance. {I}n {A}cer{K}is neurons, the increased effect of acetylcholine related to the reduced acetylcholinesterase activity is compensated by expressing higher density of n{AC}h{R}s permeable to calcium. {I}n {K}dr{K}is neurons, changes in the biophysical properties of the {L}1014{F} mutant sodium channel, leading to enhance overlap between activation and inactivation relationships, diminish the resting membrane potential and reduce the fraction of calcium channels available involved in acetylcholine release. {T}ogether with the lower intracellular basal calcium concentration observed, these factors increase n{AC}h{R}s sensitivity to maintain the effect of low concentration of acetylcholine. {T}hese results explain the opposite effects of the insecticide clothianidin observed in {A}cer{K}is and {K}dr{K}is neurons in vitro and in vivo. {P}errier et al. examine the neurons of mosquitoes following the development of insecticide resistance-associated point mutations in the voltage-gated sodium channels and {AC}h{E}1 genes for two resistant strains, {K}dr{K}is and {A}cer{K}is. {T}heir results show that n{AC}h{R}s and the intracellular calcium concentration provide a compensatory mechanism for {A}cer{K}is and {K}dr{K}is neurons to insecticide exposure.},
  keywords = {},
  booktitle = {},
  journal = {{C}ommunications {B}iology},
  volume = {4},
  numero = {1},
  pages = {665 [16 p.]},
  year = {2021},
  DOI = {10.1038/s42003-021-02192-0},
  URL = {https://www.documentation.ird.fr/hor/fdi:010082276},
}