Swimmeret mechanostimulation initiates an abdominal extension program which includes flexion inhibition. Agonists and antagonists were used to examine the GABAergic nature of inhibitory responses recorded intracellularly from a flexion producing interneuron (FPI 303) and flexor motor neuron (f3) pair, and extracellularly from the other flexor efferents. The GABA antagonist picrotoxin (PTX) enhanced spontaneous flexion. As PTX levels increased, the swimmeret evoked response shifted from inhibition of flexion (less than 10 microM), to inhibition followed by excitation (10-30 microM), to flexion excitation (greater than or equal to 50 microM). The irreversibility of PTX effects, and the absence of bicuculline or baclofen induced changes in flexion activity, suggests that the receptors differ from mammalian GABA receptors. Both GABA and its agonist muscimol suppressed flexion activity and reduced intracellular potential amplitudes. Proof that PTX acts by binding the GABA receptor was obtained by observing that the addition of GABA or muscimol to preparations pretreated with PTX did not affect either spontaneous or swimmeret evoked activities, or intracellular potential amplitudes. These results imply involvement of GABAergic interneurons in the abdominal motor programs which inhibit flexion.