Dopamine Plays A Role In The Development Of Schizophrenia

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).

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

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,

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).

Furthermore Parkinson’s disease, which is associated with a depletion of dopamine display behaviours characteristic of schizophrenia when given too much L-DOPA, a dopamine stimulant (Gershon, Angrist, and Shopsin, 1977 as cited in Kalat, 1992). In addition if schizophrenics are given drugs such as L-DOPA their symptoms are heightened. (Kalat, 1992).

Schizophrenia is one of the disorders that have been debated over the years also it has a difficult past and it is a psychological disorder that is noticeable by numerous diminished thinking, behaviours and emotions. The individuals who suffer from schizophrenia they usually hear voices in their head, have unusual beliefs but not based on reality and have different thoughts that are based on hallucination and delusions also changing in behaviour. However, even this very day the cause of schizophrenia is still unknown. Yet the psychologist states that the cause of the disorder is the combination of genetic and environmental factors. Schizophrenia is one of the most serious mental health disorders and it is treated with combination of

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).

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 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

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)

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.

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.

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.

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,