In this work we have found  a key role for BDNF-TrkB signaling in the upregulation of GluN2B function and localization in hippocampal synapses associated with the facilitation of LTP and with hyperexcitability during status epilepticus, an action that involves synaptic accumulation of GluN2B mediated by activation of protein kinase C (PKC). The gene discussed is BDNF; the disease is status epilepticus.