CAS PS 231 Lecture Notes - Lecture 9: Glutamate Hypothesis Of Schizophrenia, Prefrontal Cortex, Antipsychotic
12 Mar 2018
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Document Summary
The role of glutamate in schizophrenia: the glutamate hypothesis of schizophrenia suggests that the problem relates partially to deficient activity at glutamate synapses. In many brain areas, dopamine inhibits glutamate release or glutamate stimulates neurons that inhibit dopamine release. Increased dopamine thus produces the same effects as decreased glutamate. These abnormalities occur in people at risk for schizophrenia. Mice with deficient glutamate receptors show abnormal behavior: further support comes from the effects of phencyclidine (pcp/angel dust, effects of phencyclidine (pcp) support glutamate hypothesis. Low doses produce intoxication and slurred speech. Larger doses produce positive and negative symptoms similar to schizophrenia (hallucinations, thought disorders, emotions loss, memory loss) Interesting model for schizophrenia in other regards also: Produce little psychotic responses in preadolescents just as schizophrenia symptoms usually begin to emerge well after puberty, so does psychotic effects of. Pcp produces severe effects for someone who has recovered from schizophrenia, including a long-lasting relapse.
