Mechanically dissociated neuronal somata from the thoracic ganglia of Locusta migratoria and Schistocerca gregaria were viable in vitro for hours and were current- and voltage-clamped to record the responses evoked by brief pressure applications of gamma-aminobutyric acid (GABA) in the presence of various modulators. The application of GABA and muscimol, but not baclofen, produced a hyperpolarization and concurrent increase in the membrane conductance. The current underlying this response reversed at -65 mV, was evoked in all cells tested and showed outward rectification. In 6 of 74 Locusta neurones but not in the neurones of Schistocerca, GABA and muscimol evoked a biphasic response. The initial, fast phase was indistinguishable from the GABA-evoked current seen in all neurones. The remaining predominant, slow and long-duration component of the response was an inward current over the membrane potential range 0 to -80 mV, increasing with hyperpolarization. The GABAA antagonists bicuculline and pitrazepin were without effect on the fast GABA response while picrotoxin was a potent blocker of both the fast and the slow GABA responses. Flunitrazepam enhanced the amplitude of the fast response by up to 70% without increasing its duration. Sodium pentobarbital enhanced both the amplitude and the duration of the fast GABA response. We conclude that the locust thoracic neuronal GABA receptor/channel complex resembles the vertebrate GABAA receptor in having associated modulatory receptor sites for benzodiazepines and barbiturates, but differs from it in terms of the pharmacology of the GABA receptor itself.