Temporal lobe epilepsy (TLE) is one of the most prevalent neurological disorders, affecting 1-3% people worldwide. As this type of epilepsy is often refractory to anticonvulsant drugs, it is crucial to advance the understanding of the mechanisms that underlie its pathophysiology. The endocannabinoid system (ECS) protects nerve cells through the cannabinoid CB1 receptor regulation of the glutamatergic neuronal excitability. As TLE patients frequently show changes in the ECS, in this study we analyze the impact of the status epilepticus in the hippocampus four weeks after administraton of the pro-convulsant kainic acid (KA). Eight-week-old C57BL/6J male mice were intraperitoneally injected with 25mg/kg KA (controls received saline injection instead). Mice were then monitored and assessed with the modified Racine´s scale during 3 hours after KA.Light and electron microscopic immunohistochemistry showed that epileptic mice displayed lower CB1 receptor optical density in the CA1 hippocampus than controls. Extracellular field excitatory postsynaptic potential (fEPSP) were recorded at the excitatory Schaffer collateral-CA1 pyramidal cell synapses. Both groups showed long-term depression (LTD) after low frequency stimulation protocol (10Hz, 10min). However, the molecular mechanisms involved were different: LTD in controls required CB1 receptors, while TRPV1 receptors were needed in epileptic mice. This receptor change at the Schaffer collateral-CA1 pyramidal cell synapses of KA mice is under current investigation.