The dopamine hypothesis suggests that overproduction or excessive release of dopamine causes schizophrenia. Evidence includes drugs that cause psychosis and increased activity in dopamine-dependent neural pathways. Critics note that drugs blocking dopamine receptors do not always reduce symptoms and neuroanatomical studies reveal variations in brain structure.
The dopamine hypothesis of schizophrenia is a theory about how people develop that mental illness. Dopamine is an important neurotransmitter in the brain that moderates basic behaviors such as motivation. This hypothesis holds that the overproduction or excessive release of dopamine is part of what causes schizophrenia. Evidence from brain imaging and pharmacology to support the hypothesis includes the observation that the drugs that cause psychosis also cause increased activity in dopamine-dependent neural pathways. Scientists disagree about the correctness of the dopamine hypothesis.
Dopamine is an important catecholamine neurotransmitter in the mammalian brain, including humans, and is essential for the neural pathways that control voluntary movement and moderate many behavioral systems. Schizophrenia is a mental illness characterized by symptoms such as hallucinations and paranoia, which often render its sufferers unable to function in everyday life. It can sometimes be treated with psychiatric drugs, many of which block specific neurotransmitter actions, changing brain chemistry. The dopamine hypothesis of schizophrenia is a medical theory that holds that this mental illness results from the malfunctioning of neurons that produce or rely on dopamine in their normal physiology.
The dopamine hypothesis comes in part from observations of the ways in which drugs used to treat mental illness work. Some drugs bind to dopamine receptors on various neurons, activating them, while other drugs bind to the same receptors but prevent them from activating. Drugs such as cocaine and many other psychoactive substances cause an increase in dopamine production which correlates with an increase in symptoms resembling schizophrenia, such as hallucinations and paranoia. Functional imaging of the brain and some pathological tests indicate increased production and circulation of dopamine even during the manifestations of schizophrenic symptoms in patients.
Dopamine is particularly important for four major pathways of interconnected neurons in the brain, including the mesocortical and mesolimbic pathways, both of which are linked to reward-seeking and motivated behaviors. In the dopaminergic hypothesis of schizophrenia, the lack of normal organization and motivation is attributed to malfunction of the mesocortical pathway, possibly spreading to the closely related mesolimbic reward pathway, which moderates normal motivation and addictive behaviors. While schizophrenia has genetic factors as well as environmental factors, proponents of the dopamine hypothesis point to a relatively high preponderance of catecholamine in the abnormal brain systems of schizophrenics.
Critics of the dopamine hypothesis of schizophrenia note that drugs that block dopamine receptors do not always reduce schizophrenic symptoms. Many of the psychoactive or psychotropic drugs used successfully to treat schizophrenia are substituted phenethylamines, a chemical group that affects receptors for many chemicals within the brain, not just dopamine. Neuroanatomical studies of schizophrenic brains reveal significant variations in the gross shape and structure of some regions, which may indicate a different origin for this disease than changes in dopamine pathways. There is no scientific consensus on the role of dopamine.
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