Dopamine Hypothesis

The Dopamine Hypothesis is the theory that the development of schizophrenia is due in part to disruption of dopamine metabolism. According to this hypothesis, excess dopamine in certain areas of the brain plays a key role in the development of positive symptoms of schizophrenia, such as hallucinations and delusions.

The hypothesis is based on the fact that drugs that block the action of dopamine (for example, chlorpromazine) are effective in treating the acute phase of schizophrenia. In addition, drugs that increase dopamine release, such as amphetamines, can cause psychotic symptoms in healthy people, similar to those of schizophrenia.

The hypothesis is that schizophrenia can be treated or alleviated by drugs that interfere with the action of dopamine as a neurotransmitter in the brain. Although this hypothesis does not explain all aspects of schizophrenia, it has spurred the development of new drugs that help control the symptoms of the disease.

The dopamine hypothesis was proposed by Canadian psychiatrist Brain Freyland in 2005. He believed that one of the causes of schizophrenia is a change in the dopamine system (it is responsible for emotions and mood). The purpose of the drugs is to influence the metabolism of dauphin (a neurotransmitter) in order to improve the well-being of patients.

However, many scientists believe that Freyland's theory has shortcomings. For example, the results of many studies show that Dauphins play an important role in the development of not only schizophrenia, but also the normal development of emotions in people (for example, love). On the other hand, there are studies that high levels of daupine lead to depression, not schizophrenia.

Some scientists believe that the cause of schizophrenia lies either in genetic characteristics,