ABSTRACT In vertebrates, L-glutamate (glutamate) is a major excitatory neurotransmitter in the brain, acting on at least three separate receptors (Fagg, 1985). In insects, there is strong evidence that glutamate is the excitatory neurotransmitter at the neuromuscular synapse (Usherwood, 1981). Since some motoneurones make central synapses (Watson and Burrows, 1982; Burrows et al. 1989), it is probable that glutamate is also released centrally. Indeed, Bicker et al. (1988) found glutamate-like immunoreactivity in the central projections of known glutamatergic motoneurones and in interneurones in the locust, and Watson (1988) has shown it to be localized at central synapses. Furthermore, isolated insect neuronal somata respond to glutamate by activation of a chloride conductance (Usherwood et al. 1980), and ionophoretic applications of glutamate in certain areas of the neuropile cause motoneurones to depolarize and to spike (Sombati and Hoyle, 1984). In cultured embryonic cockroach brain neurones, Horseman et al. (1988) found both excitatory and inhibitory responses to glutamate. Wafford and Sattelle (1989) found only hyperpolarizing responses to glutamate on the fast coxal depressor motoneurone soma in situ, but they recorded depolarizing responses to kainate and quisqualate. These experiments indicate that receptors for glutamate are present on insect neuronal somata. However, since insect neuronal somata play no role in synaptic transmission and are generally not electrically excitable (Gwilliam and Burrows, 1980), the function of somal neurotransmitter receptors is unclear. To study the role of putative neurotransmitters in mediating or modulating normal synaptic inputs it is necessary to apply the substances to the neuropile where the synapses are and to record the effects there. It is also necessary to use an animal preparation where normal synaptic inputs can be recorded. In this study, the effects of topical pressure applications of glutamate were monitored by means of intracellular recordings, in the neuropile, from flight motoneurones (FMNs) during fictive flight behaviour. While this procedure does not ensure that only synaptic receptors are activated, it does enable one to activate synaptic receptors or study the effect that extrasynaptic receptors have on synaptic activity.