Biochemical Factors

  • Post-mortem and PET scans have shown that people with schizophrenia have abnormally high levels of the neurotransmitter dopamine.

  • These findings led to the development of the dopamine hypothesis, which states that synapses that use dopamine as a neurotransmitter are overactive in the brains of people with schizophrenia

Dopamine hypothesis:

  • Support for this hypothesis comes from various sources -

Drugs

  • Phenothiazines (drugs that act by blocking dopamine at the synapse) are effective in alleviating some of the major symptoms of schizophrenia

  • Clozapine, a drug that is one of the most clinically effective treatments for schizophrenia has been shown via PET scans to occupy dopamine receptor sites to the same extent as other neuroleptic drugs (used mainly to treat patients with psychotic conditions)

  • L-dopa (a drug used to treat Parkinson's disease) acts by increasing dopamine levels and it can produce symptoms of schizophrenia in previously unaffected individuals

  • Amphetamines (stimulant drugs that act by increasing the availability of dopamine and noradrenaline in the brain) can also induce symptoms of acute paranoid schizophrenia in previously unaffected individuals and increase the severity of symptoms in diagnosed cases

    • So researchers realised that if Amphetamines induce psychosis by increasing dopamine activity and antipsychotic medication reduces dopamine activity, then an increase in dopamine must be responsible for the psychotic symptoms in schizophrenia

Evidence for…

  1. Antipsychotic drugs reduce the symptoms of schizophrenia by blocking dopamine receptors. This suggests that it’s the overactive dopamine receptors causing the symptoms

  2. Drugs like amphetamines, which increase dopamine function, can sometimes cause schizophrenia-like symptoms in people without schizophrenia

Evidence against…

  1. Antipsychotic drugs only work on the positive symptoms of schizophrenia, e.g hallucinations. This means increased dopamine function doesn’t explain negative symptoms like social withdrawal

  2. The link with dopamine is correlational, so it doesn’t show cause and effect. It may be that increased dopamine function is a symptom of schizophrenia, rather than a cause of it

Glutamate:

  • Recent research is focused on a neurotransmitter called glutamate, if glutamate activity is reduced it paves the way for the increase in dopamine levels

  • This link between glutamate receptor malfunction and Schizophrenia can also account for the timing of the onset of schizophrenia.

  • There are major developmental changes in the brain during adolescence and it would appear that disruption to normal glutamate functioning leads to many deficits seen in schizophrenia

Neurotransmitter Dopamine:

  • When dopamine is released it needs a specific receptor on the receiving neuron for it to have an effect

  • There are several different receptors and interest was focused on one called D2

    • However, it was found that in a certain brain area (prefrontal cortex) there were only D1 receptors so it cannot only be D2 receptors involved in schizophrenia.

  • In addition, the activity of dopamine in this region seemed to be low rather than high

    • This suggests that reduced dopamine in the frontal parts of the brain might be causing the negative symptoms while increased dopamine in other regions is causing the positive symptoms.

Post-mortem:

  • Post-mortem - has shown that people with schizophrenia have an increased level of dopamine receptors in parts of the brain

  • Seeman 1987 found an increase in dopamine receptor density of between 60 and 110 per cent compared to controls

  • Post-mortem - examinations have usually been out on people who have taken neuroleptic drugs for years. Therefore it’s difficult to tell whether increased dopamine levels are the result of drug therapy rather than the cause of schizophrenia.

  • Dopamine is likely implicated in causing schizophrenia but this is an oversimplified explanation on its own

Issues:

  • Phenothiazines - do not work for everyone and they tend only to alleviate the positive symptoms and not the negative symptoms

  • L-dopa - also does not worsen all cases

  • Post-mortem - examinations have usually been out on people who have taken neuroleptic drugs for years. Therefore it’s difficult to tell whether increased dopamine levels are the result of drug therapy rather than the cause of schizophrenia.

  • Dopamine is likely implicated in causing schizophrenia but this is an oversimplified explanation on its own

Evaluation:

  • Research suggests that many of the positive symptoms seen in schizophrenia are the result of excessive dopamine activity and support the dopamine hypothesis.

  • But it is also clear that this is not the whole story and disruption to other neurotransmitters such as glutamate plays an important role.

  • Therefore, evidence for the dopamine hypothesis is best described as mixed.