Neonatal nociceptive circuits and dorsal horn cells are characterised by an apparent lack of inhibitory control: receptive fields are large and thresholds low in the first weeks of life. It has been suggested that this may reflect immature GABA_A receptor signalling whereby an early developmental shift in transmembrane anion gradient is followed by a longer period of low Cl- extrusion capacity. To investigate whether functional GABA_AR-mediated inhibition does indeed undergo postnatal regulation at the level of dorsal horn circuits, we applied the selective GABA_A R antagonist, gabazine, to the spinal cord in anaesthetised rat pups [postnatal day (P) 3 or 21] while recording spike activity in single lumbar dorsal horn cells in vivo. At both ages, blockade of GABA_A R activity resulted in enlarged hind paw receptive field areas and increased activity evoked by low and high intensity cutaneous stimulation, revealing comparable inhibition of dorsal horn cell firing by spinal GABA_A Rs at P3 and P21. This inhibition did not require descending pathways to the spinal cord as perforated patch clamp recordings of deep dorsal horn neurones in P3 spinal cord slices also showed an increase in evoked spike activity following gabazine. We conclude that spinal GABAergic inhibitory transmission onto single dorsal horn cells in vivo is functional at P3 and that low Cl- extrusion capacity does not restrict GABAergic function over the normal range of evoked sensory activity. The excitability of neonatal spinal sensory circuits could reflect immaturity in other intrinsic or descending inhibitory networks rather than weak GABAergic inhibition.