Thoracic complete Spinal Cord Injury (Th-SCI) produces physiological changes in the hindlimb somatosensory cortex (S1HL), which we have characterized as neuronal network hyperexcitability. Moreover, we have found a decreased GAD67 labeling intensity in the infragranular layers of S1HL in chronic Th-SCI. However, it is unknown how decreased labeling of GAD67 could be related to altered inhibitory function of GABAergic interneurons across cortical layers after SCI. The present work has two aims: characterize the physiological effect of a chronic Th-SCI over the different GABAergic neuronal populations at each cortical layer; and elucidate the functional relation between the cortical hyperexcitability and GABAergic activity after chronic Th-SCI. To achieve this, the GCaMPf6, a marker of intracellular calcium activity, was expressed in the GABAergic populations of each cortical layer within S1HL. GABAergic activity was studied using epi-fluorescent microscopy in cortical slices from control and SCI animals. Moreover, we studied the electrophysiological activity from the six cortical layers in animals before and after SCI, by analyzing the ranges of frequencies of spontaneous activity and the magnitude of evoked responses in head-restrained awake animals.Our results show that in animals with SCI, the activity profile of GABAergic neuronal populations was differently modified across cortical layers, in which supragranular layers were more active than infragranular layers. Moreover, we demonstrate that SCI increases high-frequency oscillations and higher firing rates of multiunit activity in the infragranular layers.In conclusion, a Th-SCI differently alters GABAergic activity of S1HL layers, which can be underlying the increased infragranular excitability observed in vivo.