Schizophrenia
Schizophrenia is a life-long disorder that affects about one percent of the population (Mueser & McGurk, 2004). The cause of this mental illness is still unclear. Studies have suggested that Schizophrenia does not arise from one factor but from a combination of genetic, environmental, and social factors (Liddle, 1987). People diagnosed with Schizophrenia struggle to deal with a multitude of symptoms that make it difficult to function (Mueser & McGurk, 2004). Antipsychotic medications are a popular treatment of the symptoms of Schizophrenia (Mueser & McGurk, 2004). Research is constantly being done to develop these medications to enhance the quality of life of those diagnosed with Schizophrenia. 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 results of these earlier studies were expounded on by research that suggested increased striatal dopamine
Dopamine establishes different levels of the neurotransmitter in both the dorsa striatal and ventral striatal-prefrontal as dopamine is released. The dopamine released in the ventral striatal determines how strenuously individuals perform repeated tasks over time and the dopamine released in the dorsa striatal determines the speed in which the actions occur (p. 645). According to Luck, Wevrick & Vitaterna (2016) dopamine plays a crucial role in reward-associated behavior such as gambling, drug use, and over-eating, hence the word dopamine is often paired with the term “pleasure system.” Associations with dopamine have been correlated with feelings of enjoyment, pleasure and rewarding experiences and the reward canal is concentrated on dopaminergic neurons located mostly in areas of the midbrains (448-449).
Had primate models to determine how the change in dopamine levels was related to mental disorders.
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.
Schizophrenic patients are thought to have higher dopamine levels in their brains (overactive dopamine system). Many antipsychotics are designed to block dopamine receptors, and bind them, helping patients to improve and experience less severe symptoms, further proving the dopamine hypothesis. It was also found that drugs that increase dopamine levels (amphetamines) have caused more psychotics symptoms. This could partially result in a few psychotic symptoms occurring in the illness (GROMISCH, 2013).
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).
The main theory concerning dopamine is that too much it can result in schizophrenia. Antipsychotic medications that are used to treat schizophrenia block dopamine receptors. The purpose of these medications is to bind the dopamine receptors to the brain, and some of their effects have helped people cope with the symptoms. (healthcommunities.com) The regions of the brain that are affected by dopamine are known as the striatum and the thalamus. Schizophrenia results have shown that in these regions in the brain, there are altered levels of D2 binding potential. Patients that have schizophrenia who do not take antipsychotic medications will have a lower thalamic D2 binding potential. So, schizophrenia patients that go untreated have a higher number of D2 receptors in the striatum. (psychcentral.com)
This paper defines schizophrenia from a biological and psychological perspective and also provides treatment to help combat symptoms of schizophrenia. This paper has three important contributions. First, by defining and expanding on schizophrenia from a biological perspective, I can identify the nature related predispositions. After expanding from a biological approach, secondly, I will analyze schizophrenia from a psychological aspect by determining if there is any environment or nurturing externals that can result to schizophrenia. Lastly, I will provide treatment details and also reveal early signs to schizophrenia. This paper is important because schizophrenia is an epic mental disease and it is crucially important to bring awareness to the public of how we can limit the illness. It is unclear whether schizophrenia have only a biological background or psychological background, but what was discovered is that both contribute to schizophrenia. Positive and negative treatment can be combatted undergoing pharmaceutical and psychotherapy,
Neuroscientists are not sure if the high levels of dopamine cause schizophrenia or the high levels are the result of schizophrenia. In addition, drugs used to treat schizophrenia are helpful only with positive symptoms but they have little or not at all effect on negative symptoms. This suggested that the causes of positive and negative symptoms are different. Generally, dopamine hypothesis is impressive and it helped developing new drugs such as clozapine, which is one of the most effective drugs and helps the patient’s life
Dopamine is one of the main hypothesized physiological causes of schizophrenia (Brisch et. al., 2014). It is involved in movement, pleasure, and cognition: all of which are impacted in schizophrenia. Dopamine is a neurotransmitter or a chemical messenger. It is in the neurotransmitter class of catecholamine and has both inhibitory and excitatory effects (Carlson, 2013). These effects are seen on the postsynaptic neuron, depending on the neuron dopamine can either be inhibitory or excitatory. Within the brain, there are three main systems that use dopamine as their neurotransmitter. These three systems are the nigrostriatal system, mesolimbic system, and the mesocortical system (Carlson, 2013).
The mesolimbic dopamine system plays a critical role in psychostimulant-induced locomotor activity (Hall, Powers & Gulley, 2009). Dopamine (DA) is a monoamine that has been long associated with the brain’s reward systems, and more recently, its effects on animal behaviour have been investigated (Barron, Sovik & Cornish, 2010). While becoming the most broadly used illicit drug world wide, Methamphetamine (MA) is an addictive psychostimulant which causes the brain to release excessive amounts of the chemical neurotransmitter DA, controlling pleasure (Carati & Schenk, 2011). It has been used to suppress food intake and most commonly, increase mental alertness and physical endurance (Seiden, 2004). When linking MA to the brain, its primary action is to elevate the levels of extracellular monoamine neurotransmitters, including dopamine, by promoting their release from the nerve endings (Xie & Miller, 2009). Evidence has shown that these drug-induced neuropathological changes might underlie deficits in cognitive behaviours in chronic MA abusers. MA preferentially increases synaptic dopamine concentrations in the mesolimbic dopaminergic system and initiates stimulating behavior (Di Chiara & Imperato, 1988). These ideas are further strengthened by data from animal studies showing that MA neurotoxicity is associated with impairments in motor learning (Daberkow, Kesner & Keefe, 2005) in rodents.
The evidence of dopamine hypothesis of schizophrenia can be supported by the experiments on the availability of D2 receptors and amphetamine studies. Furthermore, studies related to antipsychotic drug treatment can demonstrate the improvement of positive symptoms of schizophrenia. The current essay will support the dopamine hypothesis of schizophrenia by using empirical research.
Approximately 22% of the American population suffers from some kind of mental disorder at any given time. (Passer and Smith, 2004) Schizophrenia is one of the most serious of these mental disorders, and there are many different kinds of treatment. While all mental disorders offer diagnosis and treatment challenges, few are more challenging than schizophrenia. It is both bizarre and puzzling, and has been described as “one of the most challenging disorders to treat effectively.” (Passer and Smith, 2004, 534)
Dopamine also can have an excitatory or inhibitory affect on neurons, depending on the postsynaptic receptor (Carlson, 2011, p. 102). Dopamine is created in the frontal lobes of the brain and is associated with our beta brain waves (Jordon, 2008, ¶14). Dopamine controls the electric voltage of the brain. Acting like a natural amphetamine, dopamine controls energy, excitement, and motivation (Jordon, 2008, ¶14). Dopamine plays an important role in many physical and psychological functions such as blood pressure, metabolism, digestion, voluntary movement,
In the figure above, the proposed mechanism of dopamine (DA) as a placebo mediator is illustrated. After a placebo has been provided to a patient, DA neurons in the ventral tegmental area (VTA) are activated, which leads to the release of DA in the ventral striatum (nucleus accumbens, NAcc) and in the prefrontal cortex (PFC). Consequently, the PFC activates disease-specific mechanisms, such as opioids for placebo analgesia, dopamine for motor improvement in patients suffering from Parkinson’s disease, and perhaps serotonin (5-HT), which relieves depressive symptoms.