Studies in a number of cortical systems have shown that the NMDA component of the EPSP is strongly regulated by GABAA-mediated inhibition. The present study explored the possibility that specificity in inhibitory circuitry could allow such regulation to occur during normal function without increasing the propensity for epileptiform bursting, which occurs with indiscriminate GABAA blockade. Specifically, the hypothesis was tested that a dendritic GABAA-mediated IPSP is present which strongly modulates the NMDA component and can be activated independently of the somatic IPSP. The experiments were performed on slices of piriform cortex in which the NMDA component of the EPSP was pharmacologically isolated by bath-applied 6,7- dinitroquinoxaline-2,3-dione. A facilitation of NMDA responses to burst stimulation of afferent fibers is described, which required GABAA blockade and served as an assay for the presence of a functionally significant GABAA input. When bicuculline was applied focally in the somatic region, the feedback IPSP was blocked with little or no increase in the NMDA component of the response to burst stimulation of afferent fibers. In contrast, when bicuculline was applied focally in the dendritic region, the NMDA-mediated response to burst stimulation was facilitated with minimal effect on the somatic IPSP, confirming the hypothesis.