Objective: Presynaptic metabotropic glutamate receptors (mGluRs) at glutamatergic synapses play a major role in governing release probability. Here, we investigated the mGluR- dependent presynaptic inhibition in the chronically epileptic hippocampus. Methods: A prolonged status epilepticus (40 min) was induced by pilocarpine in 30-days old rats and terminated by diazepam. Control rats received saline instead of pilocarpine. After pilocarpine-treated rats had developed spontaneous recurrent seizures, extracellular excitatory postsynaptic potentials were recorded from the medial perforant path-granule cell synapse and the Schaffer collateral-CA1 synapse. Results: The specific group II mGluR agonist (2S,2'R,3'R)-2-(2',3'-dicarboxycyclo-propyl) glycine (10 mM) significantly depressed medial perforant path-evoked responses in control slices, but significantly more so in epileptic tissue. This depression was accompanied by a significant increase of the paired-pulse ratio in both animal groups, indicating a presynaptic mechanism. At the Schaffer collateral-CA1 synapse, the group III mGluR agonist L-(+)-2- amino-4-phosphonobutyric acid (50 mM) had no effect in controls, but significantly depressed field potentials in slices from pilocarpine- treated animals. Again, this depression in epileptic tissue was accompanied by a significant increase of the paired-pulse ratio. Conclusion: These results demonstrate that chronic epilepsy may lead to enhanced function of presynaptic glutamate receptors in the hippocampus – at least in the medial perforant path and the Schaffer collaterals.