Evaluation: Neurotransmitters as an Explanation for Schizophrenia (the Dopamine Hypothesis)

Katie Greensted
Mind Map by Katie Greensted, updated more than 1 year ago
Katie Greensted
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A level Psychology (Clinical Psychology) Mind Map on Evaluation: Neurotransmitters as an Explanation for Schizophrenia (the Dopamine Hypothesis), created by Katie Greensted on 06/01/2019.

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Evaluation: Neurotransmitters as an Explanation for Schizophrenia (the Dopamine Hypothesis)
  1. Introduction
    1. The dopamine hypothesis suggests that schizophrenia may be caused by an increased level of dopamine at the dopamine synapse. At the synapse, vesicles hold dopamine neurotransmitters until an electrical impulse is sent down the axon, triggering the vesicles to release the dopamine into the synaptic gap.
      1. This idea is supported by research on amphetamines, which are drugs found to cause excess dopamine levels, resulting in psychotic symptoms similar to those of Sz.
        1. Timmons and Hamilton found that high doses of amphetamines resulted in acute psychosis resembling schizophrenia in clinically normal people, suggesting that hyperdopaminergia is linked to symptoms of Sz.
          1. Contrastingly, Depatie and Lal found that increased dopamine levels does not always link to psychotic symptoms. They found that a drug which is a dopamine agonist (stimulates the release of dopamine) does not induce Sz symptoms in non-psychotic patients, nor did it exacerbate them in psychotic patients. This suggests that dopamine may not be the primary cause of schizophrenia and its symptoms.
          2. However, many of the symptoms amphetamines produce are more symptoms of mania rather than schizophrenia, such as overconfidence and high alertness, which could suggest that the evidence does not fully support the explanation.
          3. Dopamine is an excitatory neurotransmitter which is involved in guiding attention, perception and thinking, and is also linked to pleasure and addiction. It is suggested that positive symptoms of Sz, such as delusions, are linked to excess dopamine activity in the mesolimbic system, whereas negative symptoms, such as flat affect, may result from hypodopaminergia (low dopamine levels) in the mesocortical pathway.
        2. Higher density of/more receptors.
          1. A higher density of receptors would mean more are being triggered by the dopamine neurotransmitters binding to them, and more sensitive receptors may mean that receptors are triggered more easily and frequently.
            1. Janowski et al gave identical doses of amphetamines to schizophrenic patients and normal controls and found that low doses produced a slight increase in psychological agitation, but substantially exacerbated symptoms among schizophrenic patients. This supports the idea that people with schizophrenia may be more sensitive to dopamine uptake.
              1. However, research has found that there is no difference in the number of dopamine receptors in those with schizophrenia and those without, refuting the idea that the density of receptors influences higher dopamine levels and therefore schizophrenia.
          2. Reduced enzyme activity
            1. Enzymes break down excess neurotransmitters in the synapse ready for reuptake to occur. If enzyme activity is reduced, excess dopamine will be left in the synapse and may continue to bind with receptors.
              1. Wise and Stein found abnormally low levels of DBH in the brain fluid of schizophrenic patients who died in accidents, which is the enzyme which breaks down dopamine after its release. This suggests that low enzyme activity may be linked to higher levels of dopamine in the synapse, and therefore perhaps schizophrenia.
            2. GABA Deficiency
              1. GABA is an inhibitory neurotransmitter which blocks dopamine from working, amongst other neurotransmitters.
                1. Low levels of GABA means that dopamine levels will not be being regulated as well and therefore levels will be higher, possibly inducing schizophrenic symptoms.
              2. Criticisms
                1. The dopamine hypothesis has been criticised for being too simplistic as it only bases its theory on a single neurotransmitter. Other people argue that there may be other important neurotransmitters, such as glutamate, which also play a role in the development of schizophrenia.
                  1. Carlsson reviewed evidence surrounding the dopamine hypothesis and suggested that other neurotransmitters, such as glutamate, should be taken into account when considering the causes of schizophrenia.
                    1. Javitt and Zukin found that PCP blocks glutamate receptors and creates schizophrenic symptoms, and that drugs which increased glutamate levels reversed this effect. This provides evidence which suggests glutamate may also have a role in schizophrenia. However, these studies were done on animals so lack generalisability to humans.
                    2. However, as the dopamine hypothesis is a reductionist theory, it fails to look at other, non-biological factors that may have an influence on the cause of schizophrenia. For example, it cannot explain why certain groups in society are more likely to develop schizophrenia than others.
                      1. Veling et al showed that Moroccan immigrants were more likely to be diagnosed with Sz than Turkish immigrants, and this correlated with the amount of discrimination felt by each group. This suggests environmental factors, such as the social causation hypothesis, influence the development of Sz, but the dopamine hypothesis ignores this.
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