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The Dopamine Hypothesis

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The Dopamine Hypothesis

Often called the ‘feel-good’ hormone, dopamine is in charge of making you feel happy, satisfied, and motivated. When you feel good because you have accomplished something, your brain experiences a dopamine spike. What occurs, though, when there is an imbalance? Could this imbalance play a role in the development of schizophrenia? This is where the dopamine hypothesis of schizophrenia enters the picture.

The dopamine hypothesis of schizophrenia

The dopamine hypothesis, first proposed by Van Rossum in 1967, is the theory that too much dopamine may cause some schizophrenic symptoms.

Dopamine is a neurotransmitter that helps the brain send messages to specific body parts. It is involved in your nervous system and allows nerve cells to send messages to each other.

Neurotransmitters bind to receptors in nerve cells after they cross a small gap between them called the synapse. Dopamine is a neurotransmitter involved in our brain’s pleasure and reward systems.

Dopamine is produced in two tiny areas of the brain, the substantia nigra and the ventral tegmental area.

  • The dopamine produced in the substantia nigra helps us trigger physical movements, including the parts of the face and mouth needed for speech. Problems with this may be responsible for the symptoms of schizophrenia, such as alogia (lack of speech) and psychomotor disturbances.

  • Dopamine produced in the ventral tegmental area is released when we expect or receive a reward. This helps both animals and humans modify their behaviour to be more likely to result in a reward or positive experience. An excess of this type of dopamine can lead to hallucinations and delusional or confused thinking, all of which are symptoms of schizophrenia.

Studies of amphetamines given to people without a history of schizophrenia showed that the effect of high levels of dopamine the drug had induced led to symptoms very similar to those of paranoid schizophrenia. Later revisions of the hypothesis stated that possibly an excess of dopamine in the mesolimbic areas of the brain and a low level of dopamine in the brain’s prefrontal cortex caused the positive and negative symptoms.

The Dopamine Hypothesis Dopamine StudySmarterDopamine, KG - StudySmarter Originals (Images from Pixabay and Canva)

How was the dopamine hypothesis developed?

In the 1960s and 1970s, research was conducted into the use of amphetamine drugs and their effect on dopamine levels within the brain. The researchers found that psychotic symptoms increased when these drugs were consumed, sparking the idea that this may help us understand how psychotic symptoms in schizophrenia patients may come to be.

The dopamine hypothesis: strengths and weaknesses

Let's evaluate the dopamine hypothesis of schizophrenia and examine its strengths and weaknesses.

Limitations of the dopamine hypothesis

The dopamine hypothesis, like any other, has its limitations. Let’s explore some of them one by one.

‘The chicken and the egg’

One problem with this explanation is that it is not certain whether a dopamine imbalance causes schizophrenia or whether schizophrenia causes a dopamine imbalance, reminiscent of the question of which came first, the chicken or the egg? Since this is unclear, it is crucial to be careful in determining cause and effect in the development of schizophrenia.

Farde et al. (1990) and Noll (2009)

Farde et al. (1990) found no difference between the dopamine levels of schizophrenia patients and control patients. This finding suggests that the dopamine hypothesis may not apply to all patients with schizophrenia. Similarly, Noll (2009) found that one-third of schizophrenic patients do not respond to medications that affect dopamine, suggesting that this hypothesis may not generalise to all patients.

Determinism

The dopamine hypothesis can be considered deterministic (the belief that factors beyond our control determine human behaviour) because it assumes that the development of schizophrenia depends on the amount of dopamine or dopamine receptors in our brains, which does not correspond to free will.Deterministic theories have their limitations, as they are not compatible with societal notions of responsibility and self-control, on which many of our legal and moral norms are based.

Strengths of the dopamine hypothesis

On the other hand, some studies are sympathetic to the role dopamine plays in the development of schizophrenia.

Parkinsons disease & levodopa

Some patients are given levodopa when treating Parkinson’s disease, a drug that increases dopamine levels in the brain. These patients are reported to experience psychotic side effects similar to schizophrenia symptoms. This supports the role that dopamine plays in the development of schizophrenic symptoms.

The Dopamine Hypothesis Parkinson's disease StudySmarterParkinson’s disease, Flaticon

Seeman et al. (2000)

Seeman et al. (2000) found that post-mortem examination of the brains of people who had schizophrenia revealed a higher number of dopamine receptors than healthy patients. This finding supports revisions to the dopamine hypothesis that increased levels of dopamine receptors are associated with schizophrenia.

Practical applications of the dopamine hypothesis

Now that we have gained some insight into the dopamine hypothesis’s theoretical aspects, let us look at how it is applied in practice.

Typical antipsychotics

The dopamine hypothesis has contributed to the development of antipsychotics for schizophrenia and several other disorders in which sufferers experience psychosis.Typical antipsychotic drugs work by blocking dopamine receptors in the brain, limiting dopamine activity. This process can help reduce positive symptoms such as hallucinations.Typical antipsychotics tend to block dopamine in all areas of the brain, not just those that cause schizophrenic symptoms. This can lead to harmful side effects.

Examples of these antipsychotics include chlorpromazine and flupentixol.

Atypical antipsychotics

Atypical antipsychotics are newer drugs that usually do not have as severe side effects as typical antipsychotics. These antipsychotics only inhibit dopamine receptors in the limbic system rather than throughout the brain. They help control the symptoms of schizophrenia without interfering other systems and potentially causing the same side effects as the previous generation of medications.Atypical antipsychotics bind to dopamine receptors and act on glutamate (an excitatory neurotransmitter) and serotonin. This means that these drugs can help with positive symptoms and reduce negative symptoms such as low mood and impaired cognitive function. Because of their effect on serotonin, these antipsychotics can also help treat some comorbidities associated with schizophrenia, such as anxiety and depression.

Evaluating practical applications of the dopamine hypothesis

  • Drug treatments such as antipsychotics, developed based on the dopamine hypothesis, help patients manage their daily lives and quality of life. These drugs are relatively easy to make and administer and can positively impact healthcare providers and the economy. This is because they help people with schizophrenia to leave treatment and return to their daily lives, such as their jobs, allowing more people to be treated.

  • While these drugs help with schizophrenic symptoms, it is essential to point out that they cannot cure schizophrenia. This means that we need more research to find a long-term solution to the disease.
  • There are some ethical questions about these drugs. In some hospitals, antipsychotic medications may be used to benefit staff rather than patients to make it easier to work with patients. This practice can lead to violations of the Human Rights Act. Antipsychotic medications can have serious side effects, such as tardive dyskinesia, a condition that involves involuntary facial ‘tics’ such as rapid blinking, chewing movements, or rolling of the tongue. Sometimes the side effects can be worse than the initial symptoms of schizophrenia.

The Dopamine Hypothesis - Key takeaways

  • The dopamine hypothesis, first proposed by Van Rossum in 1967, is the theory that high dopamine levels may cause schizophrenic symptoms.
  • In the 1960s and 70s, researchers studied amphetamines and their effect on dopamine levels in the brain. Researchers found that psychotic symptoms increased when these drugs were used. This finding gave us the idea that this could help us understand the cause of psychotic symptoms in schizophrenia patients.
  • Dopamine is produced in two tiny areas of the brain, the substantia nigra and the ventral tegmental area. The dopamine produced in the substantia nigra contributes to our ability to make physical movements, including speech.
  • Problems with this may be responsible for the symptoms of schizophrenia, such as alogia and psychomotor disturbances.
  • Dopamine produced in the ventral tegmental area is released when we expect or receive a reward. This helps both animals and humans change their behaviour to be more likely to result in a reward or positive experience. An excess of this type of dopamine can lead to hallucinations and delusional or confused thinking, which are all symptoms of schizophrenia.

Frequently Asked Questions about The Dopamine Hypothesis

The dopamine hypothesis, first proposed by Van Rossum in 1967, is the theory that high or low levels of dopamine may cause some schizophrenic symptoms.

The dopamine hypothesis explains schizophrenia but does not fully explain how the disorder develops. Newer antipsychotics that are generally more effective than previous drug treatments target more neurotransmitters than just dopamine, suggesting that it may not exclusively be dopamine that causes schizophrenia.

The original dopamine hypothesis states that too much dopamine within an individual's brain causes the onset of schizophrenic symptoms such as hallucinations.

Some psychologists have suggested that having too much dopamine can cause some symptoms associated with schizophrenia. However, this is not true for all patients.

Final The Dopamine Hypothesis Quiz

Question

What is dopamine?

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Answer

 A neurotransmitter associated with the rewards system of our brains.

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Question

How was the dopamine hypothesis developed?

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Answer

Studies into the effects of amphetamines in the 1960s and 1970s discovered that dopamine can cause schizophrenic symptoms in neurotypical individuals. This sparked research that resulted in psychologists finding links between dopamine levels and schizophrenia.

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Question

What is a synapse?


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Answer

A small gap between neurons across which messages are fired.

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Question

Who first proposed the dopamine hypothesis?

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Answer

Van Rossum.

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Question

Where is dopamine produced in the brain?

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Answer

The substantia nigra and ventral tegmental area.

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Question

What did later revisions of the dopamine hypothesis include?

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Answer

Later revisions of the hypothesis state that it may be excess dopamine in the mesolimbic areas of the brain and low dopamine in the prefrontal cortex of the brain that cause positive and negative symptoms.

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Question

Why must we be careful when establishing cause and effect in schizophrenia using this hypothesis?

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Answer

Because it is unclear whether high levels of dopamine cause schizophrenia or schizophrenia causes high levels of dopamine.

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Question

What did Farde et al. (1990) find in their study into the dopamine hypothesis?

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Answer

No difference in dopamine levels between schizophrenic and non-schizophrenic participants.

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Question

The dopamine hypothesis is a deterministic theory. Why is this a limitation?

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Answer

Deterministic theories have their limitations, as they are not compatible with societal notions of responsibility and self-control, on which many of our legal and moral norms are based.

Show question

Question

What is the strength of the dopamine hypothesis?

Show answer

Answer

Some patients are given levodopa when treating Parkinson’s disease, a drug that increases dopamine levels in the brain. These patients are reported to experience psychotic side effects similar to schizophrenia symptoms. This supports the role that dopamine plays in the development of schizophrenic symptoms.

Show question

Question

What is the difference between typical and atypical antipsychotic medications that impacts why they work differently for different people?

Show answer

Answer

Typical antipsychotics only target dopamine, whereas atypical antipsychotics also affect other neurotransmitters such as serotonin and glutamate.

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Question

Which type of antipsychotic tends to have more severe side effects?

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Answer

 Typical.

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Question

Are antipsychotics able to cure schizophrenia for good?

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Answer

No, they can only help reduce symptoms so that patients can return to normal life.

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Question

What positive effect do antipsychotics have on the economy and healthcare providers?

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Answer

Using antipsychotics to treat schizophrenia is good for the economy because they are relatively easy to produce and administer while allowing people to return to work. For healthcare providers, it is also beneficial as it frees up space in hospitals to treat more people.

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