Biological explanation of schizophrenia (neurotransmitters)

Question 1

what is a neurotransmitters?

Answer 1

They are nerve cells that carry messages. The tiny gap between nerve cells are called synapses Neurotransmitters are chemicals that transmit messages across synapses.

Question 2

What has dopamine as a neurotransmitter?

Answer 2

Dopaminergic neurons have dopamine as a neurotransmitter and these may be overactive in individuals that suffer from schizophrenia.

Question 3

What does the dopamine hypothesis say about dopamine neurons?

Answer 3

A number of neurotransmitters have been linked to the symptoms of schizophrenia and says that the overactivity in the dopamine neurons leads to excessive dopamine production. Excess production of the neurotransmitter dopamine in the brain is linked to the symptoms of schizophrenia.

Question 4

What causes patients to overreact?

Answer 4

Hypersensitivity of a certain dopamine receptor (D2 receptors) in the brain, means that patients with the disorder are likely to ‘overreact’ to the presence of the neurotransmitter.

Question 5

What does the presence of excess dopamine receptors at at the synapses cause?

Answer 5

• It causes symptoms of schizophrenia. It explains why hallucinations may occur as the brain is too active.
• It is also possible that the increase in dopamine in one site of the brain contributes to positive symptoms and in another site negative symptoms.

Question 6

What does Davis et al. (1991) state?

Answer 6

• Over stimulation of dopamine in the mesolimbic pathway is thought to be linked to positive symptoms of schizophrenia (Hyperdopaminergia) such as hallucinations.
• Under stimulation of dopamine in the mesocortical pathway is thought to be linked to negative symptoms of schizophrenia (Hypodopaminergia).

Question 7

Too little dopamine?

Answer 7

• Without dopamine movements become slower so it takes longer to do things.
• Patients with Parkinson’s disease don’t have enough of the neurotransmitter dopamine.
  Symptoms of Parkinson’s are tremor, rigidity and slowness of movement.
• The drug L-dopa raises dopamine activity. However, individuals with Parkinson’s develop schizophrenic symptoms if they take too much L-dopa.

Question 8

Supporting evidence

Answer 8

STRENGTH

Gjedde and Wong (1987) found through PET scans that there are more than twice as many dopamine receptors in the brains of people with SZ compared to controls. Post-mortem (after death) examinations show patients with schizophrenia have more dopamine receptors in the left amygdala (Falkai et al., 1988) and the caudate nucleus (Owen et al., 1978).

Question 9

Challenging evidence

Answer 9

WEAKNESS

Amphetamines may increase positive symptoms, but they are effective at reducing negative symptoms, while some antipsychotic drugs are effective at alleviating positive symptoms but not negatives.

Question 10

Other explanations

Answer 10

WEAKNESS

The contemporary study into schizophrenia by Carlsson et al. (1999) suggests a different explanation: the Glutamate Hypothesis. Glutamate is another neurotransmitter linked to attention and memory. Schizophrenia symptoms seem to be linked to low levels of glutamate – perhaps because glutamate regulates dopamine, so when glutamate is blocked, dopamine levels become abnormal.

One of the most effective antipsychotic drugs for treating schizophrenia is clozapine which affects serotonin activity. Serotonin is another neurotransmitter linked to mood. This suggests that other neurotransmitters may cause schizophrenia. This is backed up by the fact that some people with schizophrenia do not respond to dopamine-inhibiting drugs.

Question 11

Usefulness

Answer 11

WEAKNESS

The dopamine hypothesis explains the mechanism by which schizophrenia occurs, but there’s still a mystery about why some people have this unusual dopamine activity going on. In other words, the dopamine hypothesis DESCRIBES schizophrenia on a biological level but it doesn’t really EXPLAIN it.

Question 12

Testable

Answer 12

WEAKNESS

Although antipsychotics alters dopamine activity immediately, the symptoms of schizophrenia may take days or weeks to disappear. This focus on drugs suffers from the treatment aetiology fallacy: the cure is not necessarily the cause. Just because drugs work by re-balancing the brain’s chemistry does not mean the brain chemistry was the cause in the first place.

Question 13

What did Randrup & Munkvad (1966) find?

Answer 13

Aim:
Study to see whether an excess of dopamine neurotransmitters may be in part responsible for schizophrenic symptoms.

Procedure:
Injected rats with amphetamines -
increased dopamine activity.

Findings:
Rats showed many of the behavioural indicators of schizophrenia including stereotypical movement.
Findings were replicated with pigeons, chickens, cats, dogs and squirrels.

Question 14

What did Liberman et al (1987) find?

Answer 14

He looked at the effect of amphetamines on patients with schizophrenia and found that they increased positive symptoms such as new symptoms or an increase in psychosis in 75% of patients. This supports the dopamine hypothesis as amphetamines mimic the action of dopamine in the brain.

Question 15

What did Owen et al. (1978) find?

Answer 15

Post mortem examinations on the brains of people who have had schizophrenia show a higher density of dopamine receptors in the brain (cerebral cortex) than people without schizophrenia.