The overall goal of this research was to induce expression of native insect ion channels in cultured Anopheles gambiae (Sua1B) cells for use in high throughput insecticide screening (HTS) without using genetic engineering. Cells were evaluated with and without 20-hydroxyecdysone (20-HE), using known insecticidal compounds to detect expression of target-site proteins. Patch clamp studies identified voltage-sensitive chloride channels (VSCC) inhibited by lindane and DIDS, both known chloride channel blockers, in untreated cells. Further, fenvalerate, a type-2 pyrethroid, inhibited VSCC current amplitude and there was an influx of labeled [14C]-guanidinium ion uptake in the presence of known sodium channel agonists; thereby exhibiting effects indicative of �electrically-silent� sodium channels. Finally, electrophysiological studies on 20-HE treated cells confirmed the expression of delayed-rectifier (Kv2) potassium channels. The ability to express native insect insecticide target sites would justify this assay for HTS and make discovery and development of new insecticides more economical.

New Investigator Award finalist: Pharmacology of native ion channels expressed in <i>Anopheles gambiae</i> (Sua1B) insect cells for screening new insecticides

248th National Meeting (2014)

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New Investigator Award finalist: Pharmacology of native ion channels expressed in Anopheles gambiae (Sua1B) insect cells for screening new insecticides