Recent Advances in Mode of Action of Insecticides

The field of insecticide mode of action has become so large that a review of this length cannot hope to be comprehensive. I have therefore attempted to clarify the current status of only a few unresolved or controversial problems and to indicate certain possibilities for future research. I have omitted any discussion of the acetylcholinesterase-inhibitory organophos­ phate or carbamate insecticides. Many other important topics and novel concepts, including juvenile hormone (JR) mimics (44, 176), anti-JRs (21, 27, 156, 157, 175), cholinergic receptor agonists (98, 172), choline acetyl­ transferase inhibitors (164), I-phenylcarbamoyl-2-pyrazolines (73), gluta­ mate analogs (76, 122), and antibodies as insecticides (142) are likewise not discussed. Recent accounts of various aspects of the mode of action of pyrethroids and DDT analogs can be cited, including effects on sodium and potassium conductance changes (135-137), structure-activity relationships (55,83,84, 134, 138), and inhibition of calcium-independent ATPases (33, 45, 50). I have focused my discussion of this group of insecticides on recent attempts to locate their primary sites of action in vivo, and to relate their mode of neurotoxic action to calcium function. Other paths traced in the present review are the aminergic theory of formamidine action, the mechanism of synaptic facilitation by cyc10dienes and y-BHC, and the question of chitin synthetase inhibition by benzoylphenyl urea insecticides. It is assumed that the reader is familiar with the most basic principles of neurophysiology.