Abstract
Pyrethroid insecticides are ubiquitous in waterways throughout the United States. Consequently, species have evolved resistance to these insecticides via receptor site mutations with unknown impacts to their fitness. The goal of this study was to determine if pyrethroid-resistant Hyalella azteca populations (Escondido and Mosher) exhibited disrupted phototaxis compared to a non-resistant population. We tested phototactic response to determine the sensitivity of H. azteca to chemicals that cause neurobehavioral impacts. H. azteca were exposed to non-dosed, permethrin (pyrethroid), and fipronil (phenylpyrazole) treatments 24 h before assessing phototaxis using light stimulus. Each population was genotyped for mutations in the voltage-gated sodium channel (VGSC) and the γ-aminobutyric acid (GABA) receptor. Non-resistant H. azteca had a faster response to light stimulus than resistant populations following the non-dosed and fipronil-dosed exposures. When exposed to pyrethroids, the Escondido population responded more rapidly than the non-resistant population. Genotyping results revealed all populations were wild-type for rdl , the gene encoding the GABA-gated chloride channel and the target for phenylpyrazole insecticides. In addition, the Mosher population shifted from homozygous for the L925I substitution in the VGSC gene ( vgsc ) to a relatively weaker I936F for pyrethroid resistance. The exact cause in the reduction in negative phototaxis and general fitness is unknown but may stem from reduced protein efficiency from the vgsc mutations or possible results of genetic bottlenecking, hence reducing genetic diversity. Benefits of adaptation may be limited to improved survivorship under harsh conditions of insecticide exposure but at a cost to overall fitness including phototactic behavior.