Temporal lobe epilepsy (TLE) is generally associated with morphological and functional changes of mesolimbic/hippocampal structures. In patients and animal models of TLE alike, the most conspicuous of these functional alterations is a decline in cognitive abilities, which in animal models is reflected in reduced spatial learning and up- or downregulation of long-term synaptic plasticity (long-term potentiation; LTP or long term depression, LTD). Beyond this, neurochemical investigations suggest that changes also occur in extralimbic structures such as thalamic dorsomedial nuclei and corpus striatum. Since the striatum is instrumental in motor planning and coordination, it is of particular interest whether motor dysfunction sometimes associated with TLE and other forms of epilepsy and clinically reported to bear dystonic or dyskinetic features is indeed due to epilepsy-associated changes of basal ganglia function. We therefore explored this question by analysing long-term potentiation in cocrtico-striatal pathways in brain slices of rats treated with pilocarpine to induce status epilepticus (SE) developing chronic epilepsy after a silent phase of 2–3 weeks. To determine whether chronic development of seizures, or SE itself wield an impact on basal ganglia function, both tissue of animals immediately (3 to 5 days; acute group) after SE, and slices of animals in the chronic phase 4–10 weeks after SE (chronic group) were investigated. We found that in the acute group rats, LTP was not significantly different among all of the three groups (control, sham, i.e. pilocarpine-treated not developing SE, and SE). In the chronic group, however, LTP was significantly enhanced the SE group versus both control and sham preparations. This LTP was biphasic, with an early, NMDA-dependent and a late, dopamine-dependent phase. We conclude that the enhancement of cortico-striatal LTP after pilocarpine-induced status epilepticus is a consequence of chronic epilepsy.