Epilepsy is a chronic neurological disorder, affecting up to 50 million people world-wide. Temporal lobe epilepsy remains one of the most difficult to treat forms of epilepsy, as one third of all patients remain refractory to anti-epileptic drugs. Temporal lobe epilepsy is usually caused by a precipitating event, such as febrile seizures, head trauma, status epilepticus, etc. This event is followed by a latent period, during which several molecular and cellular changes occur, and eventually lead to the formation of an epileptic network, that gives rise to a condition with spontaneously recurring seizures. Recent studies have shown that hippocampal Deep Brain Stimulation (DBS) can efficiently suppress these spontaneous seizures. Despite these promising results, the precise mechanism of action of DBS remains undetermined. In this animal experimental study, we evaluated the seizure suppressive effect of deep brain stimulation at different stages after the initial event. Rats (n=32) were implanted with a bipolar DBS electrode in the right hippocampus and a bipolar EEG recording electrode in both hippocampi. After recovery from surgery, all rats were subjected to a status epilepticus (SE), that was elicited through intraperitoneal injections of kainic acid (KA). Immediately following SE, one group (n=16) was subjected to DBS (Poisson Distributed Stimulation, 130Hz, 100ms pulse width) during 70 days; the other group received sham stimulation. Continuous EEG was recorded throughout the entire experiment, to evaluate the latency to the first seizure after SE, and evaluate seizure frequency during the first 20 days, and during the last 15 days of the experiment. The mean latency for the first seizure to occur after the start of the SE was the same in control (9 ± 3 days) and DBS treated rats (9 ± 8 days). During the first 20 days after SE, seizure frequency was not different in control and treatment group (1 Sz/day). During the last 15 days of the experiment, there is a significant difference in seizure frequency in the control group (11 ± 1 Sz/day) vs the treatment group (3 ± 1 Sz/day). In kainic acid treated rats, hippocampal deep brain stimulation does not prevent seizures from occurring in an early phase after SE. Hippocampal deep brain stimulation does affect seizures occurring in a later stage when rats exhibit spontaneously recurring seizures. These results suggest that hippocampal deep brain stimulation using a specific set of stimulation parameters is effective after a longer period of stimulation in this model at a time when the epileptic network is fully developed.