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Most spinal cord injury (SCI) patients suffer from chronic pain. Effective therapy for this pain is lacking, and the underlying mechanisms are poorly understood. The spinal superficial dorsal horn (SDH) contains neuronal circuits capable of modulating primary afferent information involved in pain processing. KCC2 is an isoform of the K+–Cl− cotransporter that contributes to the regulation of transmembrane anion gradient which plays a key role in shaping GABAA receptor-mediated signalling in the CNS. We tested the hypothesis that SCI causes down-regulation of KCC2 distal to the injury and contributes to the neuronal hyperresponsiveness and pain-related behaviours. SCI was a hemisection at T13 level of adult Sprague–Dawley rats. Spinal sagittal slices with attached dorsal roots (DR) were prepared from L4 to L6 level. The reversal potentials of GABA responses (EGABA) and DR-evoked IPSPs and EPSPs of L4-6 SDH neurones in sham-operated and SCI rats were compared using gramicidin-perforated patch-clamp recordings. Here we report that thoracic SCI-induced down-regulation of KCC2 in the lumbar SDH parallels the development of allodynia. The subsequent changes of EGABA in SDH neurones attenuate the GABAA receptor-mediated inhibitory synaptic transmission. These changes cause certain normally subthreshold primary A and C fibre inputs to evoke action potential output in SDH neurones. We conclude that SCI induces KCC2 down-regulation and subsequent changes of EGABA in the SDH below the injury site. The resulting disinhibition unmasks normally ineffective SDH neuronal circuits and may contribute to the below-level central pain-related behaviours after incomplete SCI.