Biochemical explanation

• Dopamine


  A neurotransmitter
• Neurotransmitter


  • A chemical substance which enables communication between 2 neurons
• Nerve impulse transmission


  Neurotransmitter moves across a small junction known as a 'synapse' to allow the nerve impulse to pass between 2 cells
• Neurotransmitter release


  Vesicles release neurotransmitter into synaptic cleft
• Neurotransmitter binding


  Neurotransmitter binds to receptors & activates them
• Neurotransmitter breakdown


  Enzymes are released to break down the neurotransmitter
• Neurotransmitter reuptake


  Excess neurotransmitter is taken up by the pre-synaptic neurone
• Neurotransmitter replenishment


  Vesicles are replenished with new & reused neurotransmitter
• Dopamine Hypothesis


  The brains of people with schizophrenia produce more dopamine than the brains of people without schizophrenia
• Excessive amounts of dopamine/dopamine receptors

  Linked to positive symptoms of schizophrenia and related disorders
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• Mechanisms


  1. Excess L-Dopa (the substance that dopamine is made from)

  2. Synapses that use dopamine may also be overactive due to differences in the number of receptors on the postsynaptic cell
• nt be
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• Drug trials


  Increasing the level of dopamine (e.g. amphetamines and cocaine)
• Participants


  • People with schizophrenia
  • People without the disorder
• Large increases in dopamine production are correlated with an increase in the reporting of hallucinations and delusions
• In people with schizophrenia, the drugs

  Cause their positive symptoms to worsen
• Parkinson's disease treatment


  Patients are often treated with a synthetic form of dopamine called L-dopa
• If Parkinson's patients' L-dopa dosage is too high


  It also creates symptoms in these individuals identical to those in people with schizophrenia, such as hallucinations
• Lindström et al., 1999: 'Patients with Parkinson's disease are often treated with a synthetic form of dopamine called L-dopa. If their dosage is too high, it also creates symptoms in these individuals identical to those in people with schizophrenia, such as hallucinations.'
• Study


  • Rats were injected with amphetamines (known to increase dopamine activity) over a 3-week period
  • Rats showed a range of schizophrenic-like behaviors (strange movements, social withdrawal)
• Rats were given drugs to block their D1 dopamine receptors


  Rat's symptoms were alleviated
• Post-mortem studies have found that the brains of deceased individuals with schizophrenia have a larger number of dopamine receptors than those without the disorder
• Wise et al. (1974) found that brain fluid from deceased patients had abnormally low levels of the enzyme that breaks down dopamine, suggesting that dopamine may have been present in excessive quantities
• Positron emission tomography (PET) scan


  Measure the amount of dopamine activity in the brain
• PET scans indicate a greater number of receptors in the striatum, limbic system, and cortex of the brain in those with schizophrenia than in those without
• Excessive dopamine activity in these areas

  May be linked to positive symptoms of schizophrenia
• Decreased dopamine activity in the prefrontal cortex of schizophrenia patients may correlate with negative symptoms such as flattened affect
• Nestler, 1997: 'Some research suggests that decreased dopamine activity in the prefrontal cortex of schizophrenia patients may correlate with negative symptoms'
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• BAC


  Antipsychotic medication
• Neuroleptics (e.g. chlorpromazine)


  Bind to DA receptors without activating them
• Effectiveness of antipsychotic medication

  • Short term beneficial effect in 75% of patients (Davis et al, 1989)
  • Long term beneficial effect in 55-60% (Davis et al, 1993)
  • Most effective against positive symptoms
  • High risk of side effects
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• Many people who were taking dopamine inhibitors (antagonists like chlorpromazine) still suffered with negative symptoms and some experienced no improvement in symptoms at all
• The dopamine deficiency hypothesis_Carlsson (2006)