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, examining how the imbalance of dopamine levels and the abundance of dopamine receptors contributes to schizophrenia.
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Jetzt kostenlos anmeldenOften 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, examining how the imbalance of dopamine levels and the abundance of dopamine receptors contributes to schizophrenia.
The dopamine hypothesis, first proposed by Van Rossum in 1967, is the theory that too much dopamine in the subcortical and limbic regions of the brain may cause positive schizophrenic symptoms. According to the dopamine hypothesis, negative symptoms are associated with less dopamine in the prefrontal cortex.
The dopamine hypothesis was later revised as research revealed schizophrenic patients might also have too many dopamine receptors.
Dopamine is a neurotransmitter that helps the brain send messages to specific body parts. Neurotransmitters are chemical messengers within the brain.
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. The receptors of dopamine are implicated in the dopamine hypothesis of schizophrenia, in that some researchers theorise too many receptors contribute to the overactivity of dopamine in the brain and any subsequent schizophrenic developments.
The dopamine hypothesis is a biological explanation of schizophrenia, so how does it work? What parts of the brain are involved in the dopamine hypothesis?
Dopamine is produced in different areas of the brain, and for schizophrenia, we are concerned with 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 some symptoms of schizophrenia, such as alogia (lack of speech) and psychomotor disturbances.
Damage to dopaminergic neurons in the substantia nigra is correlated with the development of Parkinson's.
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 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 contributes to positive symptoms, and a low level of dopamine in the brain’s prefrontal cortex contributes to negative symptoms.
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 dopamine may help us understand how psychotic symptoms in schizophrenia patients may come to be.
The dopamine hypothesis has been around for close to 60 years, and has gone through a series of developments alongside facing scrutiny in research. Let's evaluate the dopamine hypothesis of schizophrenia and examine its strengths and weaknesses.
The dopamine hypothesis, like any other, has its weaknesses.
On the other hand, some studies are sympathetic to the role dopamine plays in the development of schizophrenia.
Now that we have gained some insight into the dopamine hypothesis’s theoretical aspects, let us look at how it is applied in practice.
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 D2 receptors in the brain, limiting dopamine activity. Blocking dopamine receptors 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, which can lead to harmful side effects.
Examples of typical antipsychotics include chlorpromazine and haloperidol.
Atypical antipsychotics are newer drugs that usually do not have as severe side effects as typical antipsychotics.
Atypical antipsychotics only inhibit dopamine receptors in the limbic system rather than throughout the brain.
They help control the symptoms of schizophrenia without interfering with 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.
Considering the practical applications of the dopamine hypothesis affect patients, it's important we evaluate it thoroughly before moving forwards.
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.
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, first proposed by Van Rossum in 1967, is the theory that high or low levels of dopamine may cause schizophrenic symptoms.
The dopamine hypothesis suggests dopamine level imbalances and too many dopamine receptors play a role in the development of symptoms of schizophrenia. However, the dopamine hypothesis 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.
Schizophrenic people may have low levels of dopamine. The dopamine hypothesis suggests both low and high levels of dopamine in certain areas of the brain may be responsible for schizophrenic symptoms. Low levels of dopamine, for instance, may result in negative symptoms.
What is dopamine?
A neurotransmitter associated with the rewards system of our brains.
What is a synapse?
A small gap between neurons across which messages are fired through neurotransmitters.
Issues with dopamine production in the ________ nigra contributes to symptoms of schizophrenia.
substantia.
What did Farde et al. (1990) find in their study into the dopamine hypothesis?
No difference in dopamine (D2) receptor levels between schizophrenic and non-schizophrenic participants.
The dopamine hypothesis is a deterministic theory. Why is this a limitation?
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.
How does Parkinson's treatment, L-Dopa, support the dopamine hypothesis?
Some patients are given levodopa (L-Dopa) 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.
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