It was originally theorized that schizophrenia was caused by excessive activation of a particular type of dopamine receptor, the D2. Drugs that block D2 dopamine function reduced psychotic symptoms, while amphetamines, which cause dopamine to be released, worsened them. This led to the use of what are called typical antipsychotic medications, which include chlorpromazine, haloperidol, and trifluoperazine.However, several newer antipsychotic medications, called atypical antipsychotic medications, are also effective that do not target the dopamine D2 receptor. Instead, these agents enhance serotonin function with much less blocking effect on dopamine. Atypical drugs include clozapine, quetiapine, risperidone, and perphenazine.
There has been recent interest in whether abnormally low numbers of NMDA glutamate receptors are involved in schizophrenia (postmortems of the brains of those diagnosed with schizophrenia show fewer of these receptors than exist in a normal brain). NMDA receptor-blocking drugs such as phencyclidine and ketamine have also been shown to mimic schizophrenic symptoms (the hallucinogen LSD has effects similar to ketamine). Ketamine has also had some success in treating bipolar disorder.