During the 20 February didactic session, we briefly reviewed the glutamate hypothesis of schizophrenia. Here are the PowerPoint slides.
Although the dopamine hypothesis is the most widely-cited explanation for schizophrenia’s symptoms, it does not explain all aspects of the schizophrenia syndrome. Further, first-line antipsychotic medications, which are designed to modify the dopamine signal, are not helpful for all people with schizophrenia. Based on these observations, we can be certain that factors other than dopamine are also important.
This presentation will introduce the neurotransmitter glutamate. Glutamate is one of the ‘amino acid neurotransmitters’ and glutamate is used as a communication signal by more cells in the brain than any other neurotransmitter. This presentation will also introduce the ‘glutamate hypothesis’ which states that many symptoms of schizophrenia may ultimately be traced to a sluggish glutamate receptor. The glutamate hypothesis also suggests medication treatments that don’t rely on the more-common mechanism of blocking dopamine receptors.