Evaluate The Dopamine Hypothesis

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

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.

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

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 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.

Newer treatments for schizophrenia symptom management focus on both the DA and the 5-HT systems in an attempt to alleviate positive, negative and cognitive symptoms (Leucht et al., 2009; Leucht, Wahlbeck, Hamann, & Kissling, 2003). The 5-HT hypothesis of schizophrenia arose from toxicologic explanations of mental illness that were popular in the 1950s (Osmond, 1958). Toxicologic explanations received their inspiration from the observation that exogenous substances could produce effects that resemble certain signs and symptoms of mental illness, such as hallucinations (Osmond, 1958). The 5-HT hypothesis arose based on the observation that hallucinogenic-effects, such as those seen with LSD administration, are mediated by 5-HT agonism, and hence, schizophrenia symptoms likely arise from a similar mechanism (Baumeister & Hawkins, 2004). However, in the 1970s, the 5-HT hypothesis of schizophrenia was almost completely replaced by the DA hypothesis, only making a comeback later with the proven effectiveness of the atypical antipsychotics, such as clozapine (Baumeister & Hawkins, 2004).

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).

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 initial indication of schizophrenia being a factor of dopamine was amphetamine consumers. Amphetamine causes several symptoms of schizophrenia including: delusions and hallucinations. In schizophrenics there is an unsteady, high amount of dopamine in the brain. Antipsychotic drugs work to lower the presence of dopamine on the brain by impeding dopamine receptors. There are two primary dopamine receptors, D1 and D2. In schizophrenic patients the latter is split into D2, D3 and D4 subtypes. Dopamine activators are found in the striatum, prefrontal cortex and limbic system of the brain. Clinical research has observed an increase of dopamine in the emotion controlling striatum through PET and SPECT brain scans. Unfortunately there is no one pinpointed cause of high dopamine levels. Many of these causes are: Agitation, anxiety, cognitive acuity, feeling of pleasure, hedonism, high energy, high libido, insomnia, paranoia and

An important topic we discussed in class is schizophrenia. The typical age of onset in schizophrenia is during the individual’s mid-20s, but symptoms can start appearing during their late teens until their early 30s (Vernon, 2015). Additionally, only 1% of the population are diagnosed with schizophrenia, regardless of their gender or demographic background, which is a unique aspect compared to other diagnoses. Numerous studies, conducted under a variety of biological etiologies, serve as evidence for schizophrenia. Theses studies include: family studies, twin studies, adoption studies, linkage studies, pregnancy studies, and viral infections studies (Vernon, 2015), but the most dominant is that of identical twins as they have a high concordance rate of 48% (Cromer 479). This means that identical twins (monozygotic twins) have a higher risk of developing schizophrenia compared to fraternal twins (dizygotic twins). Additionally, neurochemistry studies examined that people with schizophrenia have more dopamine receptors, especially D-2 receptors, causing them to have “problems [with] attention, perception, and thought” (Cromer 481). This is known as the dopamine hypothesis which is important because researchers initially thought that it was too much dopamine that led to schizophrenia, but numerous studies verified that this idea was false and rather, that it was an overactive dopamine system that produced more dopaminergic activity. Specifically, through drug testing,

Antipsychotic agents are the most commonly used treatments for schizophrenia. However, more than two-thirds of patients suspended antipsychotic treatment in 18 months. [8] Although the drug is unlikely to be due to various factors in patients with schizophrenia, not all of these factors are a problem, such as negative attitude towards drugs. There was a questionnaire consisted of six questions about adverse events. The first question is whether the patient was suffering from any adverse events. The last question aimed to check whether the patient's reaction and other adverse events tolerated a specific or let them have changed their medicine. Multiple answers were about he patients’ toleration of the cause of specific symptoms. The

Antipsychotic – Psychotropic drugs are often used for neurochemical problems, behavioral problems, schizophrenia, and other mental disorders. These drugs sometimes cause side effects

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

Schizophrenia is a type of brain disorder that has been the center of attention in the past decade. Schizophrenia is such a complex disorder, its exact pathophysiology is unknown. Studies illustrated that neural circuits, functional deficits and the dysregulation of multiple pathways on different points of the brain all contribute to the pathophysiology of this disorder [1]. Strong evidence suggests the interaction of dopaminergic, GABAergic, glutamatergic, and cholinergic neurotransmitter systems play a role in the pathophysiology of this disorder [2]. For several decades, Involvement of dopamine neurotransmitter (DA), has dominated schizophrenia theories. However, it can’t explain the biological bases needed

To What Extent Neurotransmitters are Implicated In Schizophrenia During the course of this essay. The effects of Schizophrenia will be discussed, and whether or not neurotransmitters have a major implication in the diagnosis of such a disease. First we will look at the neurotransmitters, and how they develop. Followed by the biological implications towards Schizophrenia.