Schizophrenia is a severe mental disorder that affects a person’s cognitive functions. People with this disorder suffer from psychosis, delusions, and apathy (Millard et al., 2021). This illness can manifest due to genetic predisposition; indeed, it is one of the factors that can provoke it. Various psychological traumas, stress, and improper nurturing can cause schizophrenia. There is a suggestion that this illness is caused by overactive dopamine activity in the human brain. It is essential to examine the role of dopamine to understand whether the level of this neurotransmitter is high or low in schizophrenia.
Dopamine is a neurotransmitter located in the nervous cells of an organism. It is responsible for pleasure, a sense of happiness, and reward. If the person acts, dopamine is produced, and positive reinforcement occurs (Kesby et al., 2018). The brain remembers what brings pleasure and joy and forces the person to do it again. Dopamine production occurs in the midbrain and is transmitted to the final brain. This neurotransmitter is vital in studying to motivate people and give a feeling of calmness.
It is essential to define the symptoms of schizophrenia to understand the activity of the psyche. There are two types of symptoms – negative and positive. Negative symptoms are apathy, alogia (poor speech), inability to receive joy, and a tendency for depression and loneliness. These expressions oppress the psyche’s activity; in contrast, positive symptoms increase the brain’s activity. These are hallucinations, unreal ideas, and making up words and events. According to the dopamine theory of schizophrenia, positive symptoms are provoked by a high level of dopamine (Martel & McArthur, 2020). Therefore, it differs in healthy patients and those who suffer schizophrenic symptoms – people with the disorder experience a higher level of this neurotransmitter. However, patients often provoke its increasing consciousness by unstoppable fantasies and dreams.
The inclination to fantasies encourages producing dopamine in a person’s organism. The patient who has schizophrenia starts to scroll the unreal ideas more, and as a result, the mood improves. Fantasies become a source of dopamine, and the person begins to fantasize often, but dreams might supplant actions. Usually, a healthy patient quickly shifts from dreams to reality, and the neurotransmitter level normalizes. However, it is hard for schizophrenic patients who cannot switch to facts and refuse to fantasize. The person continues to wander in dreams, and it stimulates dopamine production to a great extent (Martel & McArthur, 2020). This substance accumulated, and the systems responsible for blocking dopamine cannot handle its overproduction and stop it.
With the flow of time, pleasant thoughts become automatic in patients with schizophrenia. The person cannot handle the fact that his attention is constantly switching to the same scenario of fantasies, and it becomes manic. At the same time, the schizophrenic patient perceives usual thoughts as unnecessary, as they do not bring joy and positive reinforcement (Kesby et al., 2018). It results in the person’s breaking away from reality, and the patient remains at the mercy of delusions and fantasies. The brain starts to malfunction and cannot differentiate between real and imaginary thoughts. Moreover, the person can experience memories that did not exist and perceive them as genuine.
Overall, there is a suggestion about a higher level of dopamine in patients with schizophrenia. It was investigated that patients who suffer from this disorder often cannot switch to reality and are given imaginary thoughts. It provokes an increasing level of dopamine in the human organism. In schizophrenia, patients sometimes consciously cause the elevation of this neurotransmitter, going into unstoppable fantasies. At the same time, for schizophrenic patients, it is hard to shift to usual thoughts, as they do not cause joy and a sense of happiness, which are provoked by the effects of dopamine.
References
Kesby, J., Eyles, D., McGrath, J., & Scott, J. (2018). Dopamine, psychosis and schizophrenia: The widening gap between basic and clinical neuroscience. Translational Psychiatry, 8(1), 2-12. Web.
Martel, J. C., & McArthur, S. G. (2020). Dopamine receptor subtypes, physiology and pharmacology: New ligands and concepts in schizophrenia. Frontiers in Pharmacology, 11(1), 2–17. Web.
Millard, S. J., Bearden, C. E., Karlsgodt, K. H., & Sharpe, M. J. (2021). The prediction-error hypothesis of schizophrenia: New data point to circuit-specific changes in dopamine activity. Neuropsychopharmacology, 1, 1-8. Web.