Evaluate The Dopamine Theory

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.

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

Neurotransmitters are chemicals made by neurons and used by them to transmit signals to the other neurons or non-neuronal cells (e.g., skeletal muscle; myocardium, pineal glandular cells) that they innervate. The neurotransmitters produce their effects by being released into synapses when their neuron of origin fires (i.e., becomes depolarized) and then attaching to receptors in the membrane of the post-synaptic cells. This causes changes in the fluxes of particular ions across that membrane, making cells more likely to become depolarized, if the neurotransmitter happens to be excitatory, or less likely if it is inhibitory.

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.

Biological theorists believe that individuals may have a genetic predisposition for the schizophrenia if a close family member has been diagnosed with the disorder. Stress during adolescent years seems to provoke the disorder among individuals who have a family history of the disorder. In addition, this theory suggests biochemical abnormalities related to the dopamine neurotransmitters may also contribute to the illness as the brains neurotransmission of the dopamine is too frequent in occurrence (Comer, 2005). CAT and MRI scans have also indicated that abnormal brain structuring may also play a role in the development of schizophrenia due to a common occurrence of enlarged ventricles within schizophrenia sufferers (Comer, 2005). Various parts of the brain may not develop for function properly which seems lead to Type II schizophrenia. Studies have also pointed towards the idea that exposure to certain viruses before birth may lead to the eventual development of schizophrenia (Comer, 2005).

Currently there are no cures for schizophrenia, but the symptoms are helped by taking antipsychotic medication. The symptoms experienced by those with schizophrenia are grouped in to three categories: negative symptoms, positive symptoms, and cognitive symptoms (Regier 1993, p.92). The positive symptoms include, hallucinations, delusions, unusual or dysfunctional ways of thinking, agitated body movements. Negative symptoms include, flat affect, reduced pleasure in everyday life, difficulty sustaining tasks, and reduced speech. Cognitive symptoms include, disruption in executive functioning and working memory, as well as reduced ability to concentrate. The etiology of schizophrenia is still debated by psychologists and neuroscientists, but factors such as neuroanatomy, and environmental influences are believed to play a key role. A genetic predisposition to schizophrenia has been established by researchers, but it remains unclear what causes the phenotype to be expressed. The most agreed upon cause of schizophrenia refers to the diathesis-stress model, which explains schizophrenia as a response to an individual’s allostatic load becoming too much for the brain to cope with. Another popular explanation amongst neuroscientists is the dopamine

The hypothesis has been developed, as users of major stimulants share similar behaviours and cognitions to those affected with schizophrenia. Individuals who abuse stimulants such as amphetamines and cocaine, demonstrate psychoses that at almost identical from acute paranoid schizophrenia ("The dopamine hypothesis of schizophrenia: focus on the dopamine receptor", 1976). Individuals suffering from amphetamine and cocaine psychoses who experience hallucinations and delusions, are shown to have vast quantities of dopamine in their brains. Dopamine is a neurotransmitter formed in the brain and crucial to the normal functioning of the central nervous system. A major dopamine circuit in the brain is the mesolimbic system and its overstimulation in this region of the brain that is responsible for many symptoms of psychosis. Brain scans and neuroimaging play a crucial role in determining the role that dopamine has on schizophrenia. To investigate the relationship between dopamine and schizophrenia, individuals with and without schizophrenia were given brain scans to collect initial dopamine D2 receptor availability and then were administered a dosage of amphetamine. After the challenge with amphetamine, subjects with schizophrenia showed an incredible increase in dopamine transmission when compared with the healthy

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.

There are primary neurological brain abnormalities in individuals with schizophrenia. According to Fusar-Poli (2009), schizophrenia is delineated by prefrontal activity and elevated striatal dopaminergic functions. These elevations in striatal dopamine activity and prefrontal cortical dysfunctions (Fusar-Poli, 2009). Along with other abnormalities in white matter as well as, having been observed in the right superior frontal gyrus, left middle frontal gyrus, bilateral parahippocampal gyrus, adjacent to the right caudate head, right thalamus, left insula, left lentiform nucleus, left fusiform gyrus, and bilateral claustrum (Antonius, 2011). The study of these findings may assist us to understand their role in the severity of the schizophrenia disorder symptoms (Antonius, 2011).

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

Researchers think that overly responsive dopamine systems might magnify brain activity in some way, perhaps creating hallucinations and other so-called positive symptoms as the brain loses its capacity to tell the difference between internal and external stimuli. For this reason, dopamine blocking drugs are often used as anti-psychotic medications in treatment. Modern neuroimaging studies show that some people with schizophrenia have abnormal brain activity in the thalamus,when patients were hallucinating for example, which is involved in filtering incoming sensory signals. Patients with paranoid symptoms showed over-activity in the fear processing amygdala. Schizophrenia seems to involve not just problems with one part of the brain, but abnormalities in several areas and their interconnections. What might be causing these abnormalities under the “iathesis-stress” model? This way of thinking involves a combination of biological and genetic vulnerabilities -diathesis- and environmental stressors -stress- that both contribute to the onset of schizophrenia. This model helps explain why some people with genetic vulnerability might not always develop schizophrenia and why the rates of schizophrenia tend to be higher with some degree of poverty or socioeconomic stress. It seems too that there is some kind of genetic predisposition for the

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.

Data collected over the years has begun to show more and more evidence as to why researchers consider schizophrenia a brain disorder. First of all, schizophrenia is genetically inherited shares a lot of similarities with Alzheimer's and Bipolar disorder. Schizophrenia has also demonstrated severe structural difference when compared to a normal human brain and often shows severe gray tissue deterioration. The final reason researchers consider schizophrenia a brain disorder is due to the dopamine hypothesis. This hypothesis states that schizophrenia is caused due to high amounts of dopamine in the brain. Something

Neurotransmitters in the brain can give researchers insight as to why people feel the way they do. Dopamine, for example, is the neurotransmitter associated with satisfaction. Activities such as watching your favorite TV show or eating your favorite food can cause the release of dopamine in the brain. Moreover, dopamine can act as a stimulant to increase communication between neurons and widen the brain’s range of effects. (Hillman). A study by Dr. Fredrik Ullen, of the Karolinska Institute, examined the dopamine receptors in “highly creative types” and found that their dopamine systems highly resemble those of people who suffer from schizophrenia. In both cases, there is a low density of dopamine receptors in the thalamus, which acts as a

Back in the early 1900's all psychoanlysists agreed that the source of psychic trauma theoretically responsible for schizophrenia was the relationship between the child and the parents (Torrey 91). Within the last thirty years, though, considerable interest has been given to the thought of infectious disease as the cause of schizophrenia. Since viruses can, and do, onlyb affect certain areas of the brain while living others unharmed, such as the rabies virus and herpes zoster virus, it could account for the bizarre symptoms in schizophrenics (Bebbington 80). Viruses mat also change the function of the brain cells without changing their structure (Bebbington 81). For example cell enzymes may be permantly disrupted by a viral infection and the cell would continue to live and show no signs of damage. Which means thar viruses could cause schizophrenia and leave no sign of it. Another intriguing fact about viruses as a possible cause of schizophrenia is the fact that they may remain latent for many years at a time, like the HIV virus before it turns into AIDS. That would be a possible explanation for the reasons behind why schizophrenia doesn't show up until later on in a persons life. Of all the thoeries that are present in today's society the one that most psychologists and psychiatrists stand by is that of biochemical facters. The center of attention throughout the last decade has been the neurotrannsmitter dopamine. Dopamine is a protein in the brain that fits