CHLORDIMEFORM - PLANT-PROTECTION BY A SUBLETHAL, NONCHOLINERGIC ACTION ON THE CENTRAL NERVOUS-SYSTEM

The physiological and biochemical mechanisms by which the formamidine pesticide chlordimeform protects plants from lepidopterous larvae were investigated using the tobacco hornworm (Manduca sexta). The lethality of chlordimeform to various life stages of the hornworm was evaluated. Eggs were not highly sensitive (LC50 = 0.1%; dipping), nor were the larvae (second-instar LD50 = 700 μg/g, fifth-instar LD50 = 406 μg/g; injection). Adults were much more sensitive (LD50 = 3.3 μg/g; injection), showing strong symptoms of excitation. However, the larvae showed reversible signs of intoxication (tremors and incoordination) at much lower doses than those needed to cause death (ED50 = 0.24 μg/g for fifth-instar), and chlordimeform sprayed on tomato plants was highly effective in reducing feeding by the larvae (50% reduction at 0.011% solution). Insects were not deterred from feeding, but rapidly showed fine tremors and dropped from the plant at chlordimeform levels much below those needed to cause direct mortality. Neurophysiological studies indicated that 10-7 M chlordimeform stimulated activity in the motor nerves of the isolated abdominal ganglia. A comparison of the potencies of five related formamidines in decreasing plant consumption, initiating tremors after injection, and in stimulating the fourth abdominal ganglion, showed a close correlation in the structural requirements for these three biological actions. Chlordimeform had no potent effect on axonal conduction in Manduca or on cholinergic synapses in the sixth abdominal ganglion of Periplaneta, and chlordimeform-induced excitation of the fourth abdominal ganglion in Manduca was not blocked by nereistoxin. We therefore conclude that this type of plant protection is afforded by a nonlethal mechanism which probably arises from motor stimulation through actions on central noncholinergic synapses. © 1979.