Research on the Relation between Schizophrenia and Dopamine

Schizophrenia is classified as a mental disorder that shows profound disruption of cognition and emotion which affects a person’s language, perception, thought and sense of self. The dopamine hypothesis states that schizophrenic’s neurones transmitting dopamine release the neurotransmitter too easily, leading to the characteristic symptoms of schizophrenia. This hypothesis claims that schizophrenics have abnormally high amounts of D2 receptors; receptors that receive dopamine, therefore resulting in a higher amount of D2 receptors binding to the receptors causing more impulses. Dopamine neurotransmitters play a

Researchers believe that dopamine plays an important part in schizophrenia. The goal of conventional antipsychotic drug therapy is to reduce the amount of dopamine, or the amount of dopamine receptor sites. They are dopamine antagonists

MDMA has been found to be useful in treating schizophrenia due to the effects in has when it saturates the 5HT2A receptors in the prefrontal cortex. This causes the MDMA to block D2 receptors in the mesolimbic area, which reduces the positive symptoms of schizophrenia, such as hallucinations. This is because the hypoactive release of DA is blocked, and the stimulatory effects on glutamate releases from 5HT2A receptors such as activated mesolimbic dopamine neurons is reduced, preventing

Schizophrenia is characterized as a psychotic disease that dramatically affects one 's nervous system to a point of where every day basic functions can be inhibited. It is defined as the loss of contact with the external environment the person is in due to delusional thoughts and hallucinations. Perception and behavior of someone plagued with this disease is notably altered and their actions can become a concern of the people around them. Like many other diseases that affect the nervous system it is not curable at the current time but it can be treated to lessen the signs and symptoms of the disease.

For the past fifty years treatment of schizophrenia has been marked by its basis on the dopamine hypothesis for schizophrenia. However, this model for the disease and its subsequent treatment have left many patients without relief or help in dealing with this disease which has lead to a search for a better model. The dopamine model lacks the recognition of a whole range of symptoms associated with the disease and therefore can not be an accurate basis for treatment. More recently, there has been a shift to the glutamate hypothesis which has been shown to more accurately characterize the wide range of symptoms experienced by patients living with this disorder as well as the possibility in improvements for drug treatments.

(2) However, there are some problems with this evidense. Amphetamines only mimic the positive symptoms of schizophrenia. They do not produce any of the negative symptoms. Likewise, anti-psychotic drugs are only affective on the positive symptoms of the disease. There is still some evidense that schizophrenics do posess higher levels of dopamine, however, these increases are only found in the striatum of the brain (7). The striatum is a region of the brain that receives its inputs from and outputs to the cortex. Injury to the striatum results in problems with intiation and control of motor behavior. (9) Also, there is evidence that the prefrontal cortex produces lower levels of dopamine. (4) The prefrontal cortex is involved in the organization and coordination of information to and from the cortex. (7)

Patients with schizophrenia resulted to having antibodies in their systems while the other group did not. (Grison, Heatherton, and Gazzaniga, 2015, p. 521). Other researchers have presented arguments of their being abnormalities in the neural transmitters. (Grison, Heatherton, and Gazzaniga, 2015, p. 521). Dopamine is one neural transmitter researchers have taken a major interest in because medication given to schizophrenics blocking the dopamine transmitters seem to help calm the severity of the symptoms of a wide number of patients. Although doctors are not yet certain of the cause of schizophrenia they are certain of the fact that people with schizophrenia have less brain tissue due to having large ventricles.

Dopamine is a neurotransmitter known to be involved in regulating mood and behaviour, amongst other things. Schizophrenia is associated with an overactivity of dopamine in the brain, and this may be associated with the delusions and hallucinations that are a feature of this disease.

Dopamine is a neurotransmitter associated with attention. Schizophrenics seem to have an increased number of D2 dopamine receptors on receiving neurons. This theory is support by the fact that Phenothiazines bind with D2 receptors and reduce positive symptoms. Another piece of supporting evidence is that Parkinson’s disease drug L-dopa, increase the level of dopamine and causes schizophrenic like symptoms in some people. However excess dopamine can only explain some types of schizophrenia, usually positive rather than negative.

Treatment of schizophrenic disorders involves taking drugs that are meant to decrease dopamine amounts in the brain and to block dopamine receptors (Morris and Maisto, 2002).

For instance, an excess of dopamine can cause schizophrenia and hallucinogenic drugs stimulate dopamine for it's main purpose as well as cocaine or adderall. Too much Dopamine can influence people to seek more adventurous lives, or too little can cause lack of motivation such as people with Parkinson's disease.

Over the years, experiments have produced evidence to suggest that dopamine plays a role in the development of Schizophrenia (Howes, McCutcheon, & Stone, 2015). Dopamine is a neurotransmitter that is produced in the substantia nigra and ventral tegmental regions of the brain. The belief that dopamine was involved in Schizophrenia arose after multiple studies performed with compounds produced an increase in extracellular concentrations of dopamine (Lieberman, Kane, & Alvir, 1987). The patients that were administered these compounds had similar symptoms to those observed from patients who were diagnosed with Schizophrenia (Lieberman et al., 1987).

Another major problem with the dopamine theory is that it only takes into consideration a single neurotransmitter and neglect the roles of other neurotransmitters in schizophrenia. The findings are inconsistent where some findings proposed that the abnormality causes the availability of dopamine transporters changed, and effect to the increased or decreased of dopamine level (Fusar-Poli, and Meyer-Lindenberg, 2012), while some other findings suggested that there are other neurotransmitter such as glutamine which involved in excitatory response in the brain has played a role in resulting cognitive deficits of schizophrenia (Stone, Howes, Egerton, Kambeitz, Allen, Lythgoe, et al, 2010). These assumptions have allowed researchers to implicate schizophrenia by using another pathway or biochemical mechanism other than dopamine hypothesis or dopaminergic

Treatment of schizophrenia may vary according to what clinicians believe to be its causes. For example, some believe (and this is backed by evidence) that the condition is caused by over activity of the dopamine system, so that the person experiences too much stimulation. Dopamine is a neurotransmitter, so that in effect too much activity is occurring in the brain. Clinicians who believe this is the case are likely to use drug therapies to correct this over activity, and will use antipsychotic drugs.

The Dopamine Hypothesis theorizes that the symptoms portrayed in Schizophrenia is can be explained by abnormal function of dopamine in the brain. There have been three versions of the Dopamine Hypothesis. The first version of the hypothesis focuses on the dopamine receptors. Antipsychotic drugs that impact the metabolization and reabsorption of dopamine where found to be effective in treating the symptoms. It was theorized that if the symptoms of a Schizophrenic episode can be treated by the use of dopamine