Glutamate Hypothesis of Schizophrenia

Professor Jeffrey Lieberman discusses the glutamate hypothesis of schizophrenia. The drug PCP acts on glutamate receptors, producing schizophrenia-like symptoms.

The second neurochemical hypothesis of schizophrenia is the glutamate hypothesis. Now glutamate is also a neurotransmitter. It's a chemical that is in the brain that is secreted into synapses and facilitates nerve impulse propagation. Glutamate stimulates a receptor, a group of receptors. Now there is a recreational drug that is frequently used called PCP, phencyclidine, angel dust. And it was observed that this drug, when people take it, makes them have symptoms, makes them act like they have schizophrenia. Turns out that PCP acts at one of the receptors that glutamate stimulates to block the affects of glutamate. As a result of that, we now believe that one of the reasons why schizophrenia occurs is because people with schizophrenia have a deficiency or a defect in this receptor and the receptor cannot be properly stimulated by glutamate.

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