Dopamine hypothesis

• The dopamine hypothesis - Positive symptoms

  Excess of dopamine in subcortex areas of the brain.

  Higher levels of D2 receptor activity -> found in PET scans
• The dopamine hypothesis - Negative symptoms


  Low levels of dopamine in the prefrontal cortex.

  Lower levels of D1 receptor activity -> found from fMRI scans.
• Evidence from amphetamines

  Curran et al

  Increases DA which worsens symptoms of people with SZ and induces them in people without.
• Amphetamines counterpoint

  Amphetamine psychosis closely mimics SZ
• Evidence from anti-psychotics

  Reduces DA and reduces the intensity of symptoms.

  Because it blocks receptors.
• Limitation: (alternative neurotransmitter)


  Neurotransmitter glutamate

  Found consistent raised levels of glutamate in btains of people with SZ from post mortem + live scanning.

  Candidate genes involved in glutamate production.
• Limitation: (Alternative explanation)

  Dopamine alone cannot explain SZ.

  Candidate genes identified for increasing risk of SZ includes genes that code for dopamine transmitters.

  Genetic link to SZ.
• Limitation: (Causality)

  It is unclear if dopamine is a cause of SZ or if it is as a result of SZ.