Their therapeutic action begins with NMDA receptor blockade, which initially inhibits hyperactive glutamate transmission but paradoxically triggers a cascade of beneficial effects: transient blocking of inhibitory GABA neurons leads to a regulated burst of glutamate that ultimately activates AMPA receptors and releases BDNF, leading to the formation of new synaptic contacts in the critical brain regions like the hippocampus and prefrontal cortex damaged in both epilepsy and depression [221,222,223]. The gene discussed is BDNF; the disease is depressive symptom measurement.