1 The responses of excitatory junctions on locust skeletal muscle fibres to iontophoretically applied L-glutamic acid and DL-ibotenic acid, a rigidly extended analogue of glutamate, were recorded by means of intracellular microelectrodes.2 Iontophoresis of L-glutamate to junctional sites produced transient depolarizations. Ibotenate applied iontophoretically to these sites usually evoked small hyperpolarizations which probably resulted from the activation of glutamate H-receptors on the extrajunctional membrane surrounding the junctions. However, at a minority ( approximately 20%) of junctions, ibotenate iontophoresis evoked transient depolarizations.3 Iontophoretically applied glutamate desensitized the ibotenate receptors, and vice versa. In experiments performed at junctional sites at which ibotenate depolarizations were absent, ibotenate had no effect on the responses to glutamate.4 Glutamate and ibotenate junctional currents had similar reversal potentials, measured under voltage-clamp, suggesting that the ionic bases for these currents are identical.5 It is proposed that the excitation caused by ibotenate results from the activation of receptors for extended L-glutamate and that these receptors co-exist on the post-junctional membranes of locust excitatory nerve-muscle synapses with ibotenate-insensitive glutamate receptors activated by glutamate in partially folded conformation.