Glu functions as a major regulatory of inhibitory tone and an excitatory agent in the brain. To achieve this, Glu activates NMDA recepotors on GABAergic, noradrenergic, and serotonergic neurons, which causes them to inhibit major excitatory pathways that innervate cerebrocortical and limbic brain neurons. Glu is then used as a transmitter and fire a recurrent inhibitory collateral to an NMDA receptor on a GABAergic neuron. If an excitatory input to the primary neurons is strong and persistent enough, it will slowly kill these neurons and prevent them from firing on other neurons. This may describe the clinical deterioration seen in some patients (manifestation of enduring symptoms, positive symptom burnout an cognitive loss)