Objective. The compromise of the hippocampal loop is a hallmark of mesial temporal lobe epilepsy (MTLE); particularly, the hippocampal output to the parahippocampal cortex is disrupted by damage of the CA1. While closed-loop deep brain stimulation (DBS) is the latest frontier to improve drug-refractory MTLE, current approaches do not restore the hippocampal loop, are designed by trial-and-error and heavily rely on seizure detection or prediction algorithms. The objective of this study is to evaluate the efficacy and robustness of bridging hippocampus and cortex via closed-loop stimulation to achieve the functional restoration of the hippocampal loop and control limbic seizures. Approach. In hippocampus-cortex slices treated with 4-aminopyridine and in which the Schaffer Collaterals are severed, we used interictal discharges originating in the CA3 to trigger stimulation in the subiculum and re-establish the hippocampus output to the cortex. Combining tools from information theory with quantification of ictal activity, we addressed the efficacy of the bridge in restoring the functional connectivity of the hippocampal loop and controlling ictogenesis. Main results. Bridging hippocampus and cortex recovered the functional connectivity of the hippocampal loop, controlled ictogenesis and proved robust to failure mimicking the functional impairment of the CA3 seen in MTLE rodent models and patients. The efficacy and robustness of the bridge stem in mirroring the adaptive properties of the CA3, which acts as biological neuromodulator. Significance. A DBS device that does not depend on seizure detection/prediction algorithms but relies on endogenous interictal patterns presents the key to advance the conceptual design of current DBS paradigms for epilepsy treatment.