To determine whether BDNF signaling is also coupled to the regulation of the synaptic expression of GluN2B in status epilepticus we analyzed the synaptic surface abundance of this NMDAR subunit in rats subjected to the pilocarpine model of temporal lobe epilepsy (TLE), under control conditions and in animals treated with ANA-12, a TrkB receptor inhibitor (Fig. 6A), thus allowing to assess the role of endogenous BDNF. This evidence concerns the gene GRIN2B and temporal lobe epilepsy.