Injury to the superficial layers of cerebral cortex produces alterations in the synaptic responses of local circuits that promote seizures. To further delineate the specific changes in synaptic strength induced by cortical injury, whole-cell recordings were used to examine evoked and spontaneous synaptic events from layer V pyramidal cells in traumatized rat neocortical slices in which the superficial third of the cortex was removed. Slices from intact neocortices served as controls. Examinations of fast inhibitory postsynaptic currents (IPSCs) indicated that traumatized slices were disinhibited, exhibiting evoked IPSCs (eIPSCs) with lower amplitudes. There was no difference in the mean amplitudes of spontaneous IPSCs (sIPSCs) recorded in traumatized vs. control slices. However, the mean sIPSC frequency was lower in traumatized slices, indicative of a decrease in GABA release at these inhibitory synapses. Traumatized slices also displayed an increase in synaptic excitation, exhibiting spontaneous EPSCs (sESPCs) with larger peak amplitudes and higher frequencies. Peak-scaled nonstationary fluctuation analysis of sEPSCs and sIPSCs was used to obtain estimates of the unit conductance and number of functional receptor channels. EPSC and IPSC channel numbers and IPSC unit conductance did not differ between traumatized and intact slices. However, the mean unit conductance of EPSCs was higher (+25 %) in traumatized slices. These findings suggest that acute injury to the superficial neocortex results in a disinhibition that stems from a decline in GABA release likely due to the loss of superficial inhibitory interneurons, and an enhancement of synaptic excitation consequent to an increase in AMPA receptor unit conductance.