Essay about The Dopamine Hypothesis of Schizophrenia

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.

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

For instance, an excess of dopamine can cause schizophrenia and hallucinogenic drugs stimulate dopamine for it's main purpose as well as cocaine or adderall. Too much Dopamine can influence people to seek more adventurous lives, or too little can cause lack of motivation such as people with Parkinson's disease.

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).

Biological theorists believe that people can inherit a disposition for Schizophrenia, according to the diathesis-stress perspective. It is also believed that biochemical abnormalities as well as abnormal brain structure could be factors in schizophrenic patients. Researchers have developed a dopamine hypothesis which explains “certain neurons that use the neurotransmitter dopamine fire too often and send too many messages, thus producing the symptoms of the disorder” (Abi-Dargham & Grace, 2011) The drugs used to combat these symptoms are known as atypical antipsychotic drugs, as they are much different from other antipsychotic medications. These drugs bind dopamine receptors to keep messages from being transmitted too quickly. Brain scans have found that many schizophrenic patients have enlarged ventricles. These patients tend to show greater cognitive disturbances. It is also believed that schizophrenia can be

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

Schizophrenia affects the brain in numerous ways, including the ventricles, limbic structures, and thinking patterns. Gray matter is lost by 25% in the brain of a schizophrenic individual. The reduction of gray matter is “evident in the parietal lobes, while the reduction occurs mostly in the temporal and frontal lobes” (Breis, 2016). As the frontal lobe is the largest area of the brain, both cognitive and emotional functioning decreases.

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 very complex and “startling disorder characterized by a broad range of cognitive and emotional dysfunctions” (Barlow & Durand, 2015, p. 477). It can greatly impact a person’s life in a negative manner: affecting physical, emotional, relational, and occupational health. The National Institute of Mental Health defines schizophrenia as a “chronic and severe disorder that affects how a person, think, feels, and acts” (National Institute of Mental Health, n.d., para. 1). It is believed to be caused by an excess of the neurotransmitter dopamine (Brisch, Saniotis, Wolf, Bielau, Bernstein, Steiner, …, Gos, 2014).

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.

This article provides information as to how the brain historically has used dopamine as an inhibitory neurotransmitter in regards to schizophrenia. The research discussed in this article focuses on a new discovery that indicates that glutamate, GABA, acetylcholine and serotonin alterations are also involved with schizophrenia’s pathology. With use of schizophrenic animal models, both dopamine receptors and the antipsychotic effects of the treatments that target them, and how they interact with other various neurochemical types of schizophrenia. The final topic the author discusses is how the human brain and mental abilities has evolved, causing many schizophrenic patients to be affected.

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

Schizophrenia is a severe mental disorder affecting about 1% of the population worldwide. Although the dopamine (DA) hypothesis is still keeping a dominant position in schizophrenia research, new advances have been emerging in recent years, which suggest the implication of white matter abnormalities in schizophrenia. In this paper, we will briefly review some of recent human studies showing white matter abnormalities in schizophrenic brains and altered

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,