Ibotenic acid [2‐(3‐hydroxyisoxazol‐5‐yl)glycine] induced a dose‐dependent increase in chloride ion conductance in locust muscle fibres which was not sensitive to 4‐aminobutyric acid (GABA). This ibotenate response became rapidly desensitised and appeared to be due to activation of extrasynaptic glutamate H receptors. 22‐23‐Dihydroavermectin B1a (DHAVM) (500 pg to 1 μg ml−1) induced irreversible increases in permeability to the chloride ion and abolished ibotenate responses. DHAVM responses were not altered when glutamate H receptors were desensitised by glutamate (1 mM) or ibotenate (100 μM). Irreversible changes in input conductance caused by DHAVM were not affected by penicillin G (1 mM) or bicuculline (1 mM), but picrotoxin (1 mM) and zinc chloride reduced DHAVM responses by 23.7 and 52.6%, respectively. It is concluded that DHAVM has a number of sites of action on locust muscle that include effects on the glutamate H receptor–chloride ion channel complex, in addition to effects on the GABA receptor–chloride ion channel previously described.