The Dopamine Hypothesis

The Dopamine Hypothesis of Schizophrenia: Definition

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.

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.

Biological Explanations of Schizophrenia: Dopamine Hypothesis

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.

Fig. 2 - Dopamine pathways show the dopamine systems within the brain.

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.

Dopamine Hypothesis of Psychosis: Development of the Dopamine Hypothesis

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: Strengths and Weaknesses

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.

Weaknesses of the Dopamine Hypothesis

The dopamine hypothesis, like any other, has its weaknesses.

• Cause and Effect: One problem with this explanation is that it is not certain whether a dopamine imbalance causes schizophrenia or whether schizophrenia causes a dopamine imbalance. Since the causal nature of the argument is unclear, it is crucial to be careful in determining cause and effect in the development of schizophrenia.
• Farde et al. (1990): Farde et al. (1990) found no difference between the dopamine receptor (D2) levels of schizophrenia patients and control patients. Farde et al.'s (1990) finding suggests that the dopamine hypothesis may not apply to all patients with schizophrenia.
• 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 psychological explanations of schizophrenia. It ignores how the environment affects the development of the disorder.Deterministic theories have their limitations, as they are not compatible with societal notions of responsibility, free will 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.

• Parkinson's Disease and Levodopa (L-Dopa): 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, such as hallucinations and dyskinesia. The dopamine aspect supports the role that dopamine plays in the development of schizophrenic symptoms.
• Abi-Dargham et al. (2000): Abi-Dargham et al. (2000) investigated whether there was a true increased level of dopamine and dopamine 2 (D2) receptors within the brain for schizophrenic people compared to controls, accounting for the effects of patients taking antipsychotics and artificially elevating their levels. They found that their results indicated, that for the levels to match up, schizophrenic patients must have an increased level of both dopamine and dopamine receptors compared to controls.

Fig. 3 - Parkinson's can be treated using levodopa which increases dopamine levels in the brain.

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 Antipsychotic Drugs: First Generation

The dopamine hypothesis has contributed to the development of antipsychotics for schizophrenia and several other disorders in which sufferers experience psychosis.

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.

Atypical Antipsychotic Drugs: Second Generation

Atypical antipsychotics are newer drugs that usually do not have as severe side effects as typical antipsychotics.

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.

Evaluating Practical Applications of the Dopamine Hypothesis

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.