Temporal lobe epilepsy is the most common form of epilepsy in adults, and can be hard to treat. Good experimental models are crucial in the search for novel treatments. The intrahippocampal tetanus toxin model of temporal lobe epilepsy yields spontaneous epileptic seizures, but differs from other models in that it does not depend on an initial period of status epilepticus and is not characterized by major neuronal loss. This lack of hippocampal sclerosis provides a model of nonlesional temporal lobe epilepsy and the early stages of lesional temporal lobe epilepsy (i.e., before the development of hippocampal sclerosis). The cellular mechanisms of the epileptic focus in this model include a dysfunction of inhibitory neurons and axonal sprouting. After 6–8 weeks of spontaneous seizure activity, most tetanus toxin-treated rats experience seizure remission. This remission is probably an active process, because the cellular pathophysiology remains. Further, in the neocortical version of the tetanus toxin model, animals fail to gain remission.