PHARMACOLOGICAL CHARACTERISTICS OF INSECT NICOTINIC ACETYLCHOLINE-RECEPTOR WITH ITS ION-CHANNEL AND THE COMPARISON OF THE EFFECT OF NICOTINOIDS AND NEONICOTINOIDS

Using radioreceptor assay with [H-3]alpha-bungarotoxin (alpha-BGT) and [H-3]phencyclidine (PCP) as probes for the nicotinic acetylcholine re ceptor (nAChR) in membranes obtained from honeybee heads, the effects of various nAChR ligands, nicotinoids and neonicotinoids were studied. The data indicated differences in pharmacological characteristics bet ween Torpedo electric organ and honeybee brain nAChRs. [H-3]alpha-BGT binds to the acetylcholine (ACh) recognition site of the nAChRs of ver tebrate skeletal muscle, Torpedo electric organ and honeybee brain. In vertebrates, [H-3]PCP binds to an allosteric site on the receptor's i on channel and its binding is stimulated by receptor activation with a gonists. However, the tested vertebrate cholinergic agonists inhibited [H-3]alpha-BGT binding, but did not activate [H-3]PCP binding to the honeybee nAChR. Saturation isotherms of the binding of [H-3]alpha-BGT with or without PCP indicated that PCP interacted with the ACh recogni tion site on the nAChR. Furthermore, nicotine inhibited not only [H-3] alpha-BGT binding but also [H-3]PCP binding. Detailed study of [H-3]PC P binding indicated that [H-3]PCP bound to the honeybee brain membrane s both at high and low affinity sites. The former corresponded to the vertebrate allosteric site on the nAChR and the latter to the ACh reco gnition site. Nicotine, anabasine and nitenpyram bound to both sites, while imidacloprid, 6-Cl-PNNI and acetamiprid bound selectively to the ACh recognition site. In houseflies, nicotine and imidacloprid produc ed excitation followed by paralysis, while PCP was anesthetic, even th ough PCP was as insecticidal as nicotine.