The increase in hippocampal excitability is one of the cardinal symptoms of temporal lobe epilepsy (TLE), the most common epilepsy type. In epileptic patients as well as animal models have been observed an increase in Dentate Gyrus excitability, which is thought to be responsible of hippocampal foci in TLE. An increase in intracellular chloride and protein level of the chloride co-transporter 1 NKCC1, which drives the electroneutral uptake of this anion, have been observed in human an animal models suggesting an excitatory GABA (aminobutyric acid) effect. Being similar to what observed in immature neurons during early development. In order to evaluate the contribution of NKCC1 to the elevated circuit excitability in chronic epilepsy, we evaluated Dentate Gyrus excitability by extracellular fi eld recordings in acute brain slice of chronic epileptic animals. This allow to not perturb the intracellular chloride concentration. Input-output relationships of synaptic and population action potentials needed less stimulation to reach saturated responses, consistent with a facilitation of synaptic transmission. The GABAergic component is also shifted toward less stimulation. Inhibition of NKCC1 by Bumetanide decreases 50 % of the amplitude of GABAergic component in epileptic slices, while only 10 % in controls. This elevated NKCC1 activity results in an excitatory GABA effect in epileptic tissue. Finally, Bumetanide was able to decrease the frequency of epileptiform-like fi ring in slices from epileptic but not control animals. In overall, these results show that NKCC1 is expressed and active in dentate gyrus of chronic epileptic animals, and its blockade is able to produce anti-epileptic effects.