The spinal network coordinating locomotion is comprised of a core of glutamate and glycine interneurons. This network is modulated by several transmitter systems including spinal GABA interneurons. The purpose of this study is to explore the contribution of GABAergic neurons to the regulation of locomotor burst frequency in the lamprey model. Using gabazine, a competitive GABA_A antagonist more specific than bicuculline, the goal was to provide a detailed analysis of the influence of an endogenous activation of GABA_A receptors on fictive locomotion, as well as their possible interaction with GABA_B and involvement of GABA_C receptors. During NMDA-induced fictive locomotion (ventral root recordings in the isolated spinal cord), gabazine (0.1 to 100 µM) significantly increased the burst rate up to two fold, without changes in regularity or "burst quality". Gabazine had a proportionately greater effect at higher initial burst rates. Picrotoxin (1 to 7.5 µM), a less selective GABA_A antagonist, also increased the frequency markedly, but at higher concentrations the rhythm deteriorated, likely due to the unspecific effects on glycine receptors. The selective GABA_B antagonist, CGP55845 also increased the frequency, and this effect was markedly enhanced when combined with the GABA_A antagonist gabazine. The GABA_C antagonist TPMPA had no effect on locomotor bursting. The spinal GABA system does, thus, play a prominent role in burst frequency regulation, in that it reduces the burst frequency by up to 50%, due presumably to presynaptic and soma-dendritic effects documented previously. It is not required for burst generation, but acts as a powerful modulator.