Comparative studies on muscle microstructure and ultrastructure of Mythimna separata Walker treated with wilforgine and chlorantraniliprole

- Wilforgine/chlorantraniliprole cause Mythimna separata feeding cessation and paralysis.
- M. separata larvae muscles are damaged by wilforgine and chlorantraniliprole.
- Site of action of wilforgine may be in muscle tissue.
- Molecular targets of wilforgine and chlorantraniliprole are different.
- This is a novel report of histopathological mechanism of wilforgine on M. separate.

We attempted to elucidate the comparative effects between wilforgine and chlorantraniliprole on the microstructure/ultrastructure of muscle tissue in Mythimna separate larvae. The typical toxicity symptoms of M. separata larvae upon wilforgine treatment was feeding cessation and flaccid paralysis, whereas feeding cessation and contraction paralysis were the main poisoning symptoms wrought by chlorantraniliprole. Light-microscopy observations showed that the microstructure of muscle tissue could be damaged by wilforgine and chlorantraniliprole, and the death of insects was associated with muscle lesions. Muscle tissue was loose after wilforgine treatment but constricted muscle tissue was observed upon chlorantraniliprole treatment. Transmission electron microscopy showed that wilforgine and chlorantraniliprole could disrupt endomembranes and plasma membranes. These results suggest that wilforgine can induce microstructural and ultrastructural changes in the muscles of M. separata larvae; the sites of action are proposed to be calcium receptors or channels in the muscular system.

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