Evaluate the Role of Chemical Transmitters in Explaining Behavioural Disorders

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

Expert’s reason that unevenness in the complicated interconnected chemical responses of the brain connecting the neurotransmitters dopamine and glutamate, and maybe others, performs a part in schizophrenia. Neurotransmitters are elements that permit brain cells to interconnect with each other. Experts are acquiring more about brain chemistry and its connection to schizophrenia. Similarly, in small methods the brains of people with schizophrenia appear diverse than those of healthful people. For instance, fluid-filled holes at the middle of the brain, called ventricles, are greater in certain people with schizophrenia. The brains of people with the disorder similarly manage to have less grey matter, and certain

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

Genetics can cause differences in brain chemistry and biochemistry may be important in the development and maintenance of schizophrenia. The dopamine

Research by Johnstone in 1994, explained the biological approach of interventions, explanation and treating of schizophrenia patients (Hansell & Damour, 2005). In studies of Fisher in 2001, discoveries that the brain had more dopamine receptors know as B_2 receptors in a person suffering from schizophrenia, than a non-suffer (Hansell & Damour, 2005). Biological findings of schizophrenia suggest that a genetic factor was hereditary, but not conclusive because the element of environment does make a difference (Hansell & Damour, 2005).

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.

Schizophrenia is a complex and highly debilitating mental illness that we are currently unable to treat in any way that guarantees success or return to previous function. It affects around 1% of the population and is associated with a thirteen-fold increase in the likelihood of suicide, so its effective control is paramount (Gogos et al., 2015). There have been several hypotheses as to the cause of schizophrenia. Many link genetic and environmental factors, and dysregulations of neurotransmitters dopamine, glutamate, and serotonin (Egbujo, Sinclair, & Hahn, 2016). The dopamine hypothesis currently suggests that hyperactive dopamine transmission in the basal ganglia leads to psychosis and underactive dopamine transmission in the prefrontal

According to James G. Hollandworth of the University of Southern Mississippi, schizophrenia is primarily characterized by a disintegration of reality perception, consciousness, and thought process which results in a debilitated proficiency in social and professional faculties (Hollandworth, 1990). While schizophrenia can most arguably be classified as a predominantly genetic affliction, there are others factors which can contribute to its development even without a genetic predisposition. These elements include birth defects such as hypoxia and low birth rate, neuroanatomical anomalies, viral infections, along with low IQ and cerebral atrophy (Hollandsworth, 1990). While these components in themselves are not sufficient enough to cause the disorder, they result in an increased risk for developing the disease. One theory for the cause of schizophrenia that has been studied with great validity is the dopamine hypothesis. This theory postulates that schizophrenia is caused by an overabundance of the dopamine-dependent areas of the brain causing an imbalance that affects the entire system (Hollandsworth, 1990). For this reason many of today’s schizophrenia treatment drugs inhibit dopamine receptor activity in an attempt to return it to its natural equilibrium. Although even with advances in modern science and new drugs being developed every day, the illness is still only treatable and its symptoms still emerge even

The main brain areas affected include the basal ganglia, the prefrontal cortex, and the limbic system. The excessive release of the brain chemical dopamine is linked to impaired function of the prefrontal cortex in people with schizophrenia. The multiplicity of symptoms seen in schizophrenic people may be an outcome of how highly connected the brain is. The prefrontal cortex is the brain region behind the forehead. This area of the brain is mainly responsible for difficult tasks including decision-making, planning and changing behaviors according to social cues or past experience. Inappropriate use of the prefrontal cortex will result in loss of these skills and the distinctive disordered thinking of schizophrenia. In fact, the prefrontal cortex is joined to a different brain area affected in schizophrenia known as the basal ganglia. This region is well known for making dopamine and controls coordinated movement, drive and the compensation pathway. This difficult pathway strengthens patterns of performance that make a person feel good. Evidence done on the human brain shows

The major support and refutation of the dopamine hypothesis has come from the examination of dopamine receptors in these regions of the brain. There are two main types of dopamine receptors, D1 and D2. However, within the category of D2 receptors, there are three subtypes, D2, D3, and D4. (5) Through PET scan analysis of dopamine usage in the brain and post-mordum molecular analysis of brain tissue, researcher were able to determine relative levels of dopamine receptors in patients with schizophrenia compared to non-schizophrenics. Overall analysis of dopamine

The vast majority of medications currently in the marketplace or under development to treat schizophrenia/psychosis focus on dopamine in one way or another. Most of the medications that are currently used to treat this condition affect dopamine in a direct way. These drugs specifically target this substance because historically, psychosis has been linked to unusually high levels of dopamine in the part of the brain that is known as the stratum (Nauert, 2010). Moreover, there is a fair amount of research that indicates there is a direct correlation between levels of glutamate, which is another substance the brain produces and is found in the hippocampus, and dopamine in individuals who eventually develop schizophrenia.

A third example of a neurological cause of schizophrenia is what is known as the dopamine hypothesis. This hypothesis is the idea that irregular levels of dopamine, in the case of schizophrenia, high levels of dopamine, are linked to some of the symptoms of schizophrenia (Eagleman & Downer, 539). This idea was thought of because of the findings on the use of amphetamines causing a rise in dopamine in the brain as well as the rise of the symptoms of schizophrenia (Seeman & Lee, 1975)( Eagleman & Downer, 538).

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).

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).

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