One possible explanation for the organic pathology causing schizophrenia is malfunctioning neurotransmitters within the victim’s brain. The dopamine hypothesis (sometimes called the dopamine hypothesis of psychosis) argues that schizophrenia is caused by highly active neurotransmitters known as dopamine. This may cause dopamine receptors to become overly sensitive or by other transmitters to begin transmitting dopamine rather than what they were meant to transmit. Specifically, the dopamine hypothesis states that positive schizophrenic symptoms are enacted by the mesolimbic pathway, associated with positive reward and addiction, while the mesocortical pathway, which while also involved in motivation and emotional response is heavily associated with normal cognitive function, is thought to be responsible for negative schizophrenic symptoms.
The dopamine hypothesis is supported by the results of applying classical antipsychotics to schizophrenic patients because these drugs, such as Thorazine, diminish schizophrenic symptoms and block dopamine receptors. It has also been observed that drugs which increase dopamine, such as amphetamines or cocaine, will sometimes create schizophrenic symptoms in healthy individuals. Furthermore, studies have shown that injecting mild schizophrenics with dopamine will cause them to experience higher degrees of schizophrenia for a short duration of time. Lastly, several genes have been found to be linked with abnormal dopamine activity and schizophrenia.
The dopamine hypothesis has faced criticism with the introduction of atypical antipsychotics, which block both dopamine and serotonin receptors but are more effective in limiting negative schizophrenic symptoms. However, some dopamine hypothesis advocates claim that atypical antipsychotics are useful because they effect dopamine receptors differently than classical antipsychotics are able.
Gerow, Joshua R., Roddrick Chatmon, and Don Crews. Basic Psychology. New York: Custom Pub., 2009. Print.