Status epilepticus (SE) is a medical emergency that can result in permanent neurological damage, particularly to the hippocampus. It is thought that there is a critical time point at which self-terminating seizures develop into self-sustaining SE (SSSE), however endogenous mechanisms of seizure termination are poorly understood. The dentate gyrus (DG) has been proposed as the gatekeeper of hippocampal excitability and is known to play a role in controlling the spread of epileptogenic activity to the seizure susceptible hippocampus. We have modified an existing model of limbic SE in order to further understand the endogenous anticonvulsive properties of the DG during the transition to SE. Stimulating and recording electrodes were implanted into the perforant pathway and dentate granule cell layer, respectively, of anaesthetised Sprague Dawley rats. A minimum of 3 days later, rats underwent continuous 3.5mA, 20Hz stimulation to induce SSSE. The perforant pathway stimulation model of SE, induced by 2 hours continuous stimulation has been used to assess seizure severity during and neuronal damage post-SE. Here, groups underwent stimulation for 30 minutes, 1, 1.5 and 2 hours, to determine the duration of stimulation necessary to induce SE in 50% of animals, thereby allowing SE entry to be increased or reduced through intervention. SE was considered to be induced when animals exhibited epileptic activity for at least 30 minutes after stimulation had ceased. The proportion of animals developing SSSE was assessed alongside seizure severity, observed as behavioural scores and spike amplitude and frequency of EEGs, both during and post-SE. 87.5% animals stimulated for 2 hours (n=8) developed SSSE. 65% of animals stimulated for 1.5 hours (n=8) developed SSSE. 50% animals stimulated for 1 hour (n=8) self-sustained and 25% animals stimulated for 30 minutes (n=8) self-sustained. In all cases seizure severity, as assessed using the Racine score, was greatest after 20-30 minutes of stimulation. These findings indicate that there is a critical time point at which self- terminating seizures become SSSE. Further development of this model will enable pharmacological manipulation of the anticonvulsive properties of the DG and so allow a further understanding of the role this region plays in the transition to SSSE.