抑制性神経シナップスを標的とする殺虫活性物質の作用機構
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All cyclodiene-resistant strains of the German cockroach, the house fly and the mosquito are also resistant to picrotoxinin, a well-known GABA antagonist. By using electrophysiological techniques, picrotoxinin was confirmed to act at a presynaptic region, resulting in a stimulation of the release of an excitatory transmitter. The electrophysiological symptoms caused by picrotoxinin were quite similar to those of γ-BHC and dieldrin. It was determined by using a ^3H-dihydropicrotoxinin binding method that the nerve membrane in CNS of the American cockroach contained a component having a high affinity toward picrotoxinin and heptachlor epoxide, which can be regarded as a picrotoxinin receptor. By using a sucrose density centrifugation technique, it was determined that the fraction sedimented at the interphase of 1.0 and 1.2 M sucrose at 100, 000×g contained the highest level of specific binding site. The ^3H-dihydro-picrotoxinin binding on the receptor was inhibited by all cyclodienes tested and γ-BHC. Toxaphene, bicyclic phosphate and TETS also bound with the receptor. Dieldrin resistant German cockroach showed cross-resistance to the chemicals having binding potencies to picrotoxinin receptor. Milbemycin and avermectin were found to stimulate Cl^- uptake by the leg muscles of the American cockroach within 4 min at 10^<-7> M. This stimulatory action could be antagonized by picrotoxinin (10^<-4> M). It was concluded that the action of milbemycin and avermectin is to open the chloride channel on the plasma membrane. Their actions do not seem to be mediated through GABA receptor, picrotoxinin receptor and benzodiazepam receptor, suggesting their direct attack on the chloride channel proper both in the central nervous and the neuromuscular systems.
- 日本農薬学会の論文
- 1987-08-20
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