Neural Correlates

• There are two types of dopamine receptors; D1 and D2
• Neural correlates


  are patterns of structure or activity in the brain that occur in conjunction with an experience. These correlates may be implicated in the origins of that experience.

  The best known neural correlate for schizophrenia is the neurotransmitter dopamine.
• Original Dopamine Hypothesis 


  Hyperdopaminergia: Schizophrenia may be the result of high levels of dopamine (DA) in the subcortical areas of the brain.For example, an excess of dopamine receptors in the pathway from the subcortex to Broca’s area (which is responsible for speech production) may explain symptoms such as auditory hallucinations.
• Updated Dopamine Hypothesis

  • Davies et al (1991) proposed the addition of cortical hypodopaminergia (abnormally low levels of DA in the cortex ).
  • Low levels of dopamine in the prefrontal cortex (responsible for thinking) could explain cognitive problems – eg. avolition
  • It has also been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia. This means both high and low levels of DA in different brain areas are part of the updated version.
• What leads to abnormal levels of Dopamine levels?

  Both early experiences of stress and genetics make some people are more sensitive to cortical hypodopaminergia and therefore subcortical hyperdopaminergia (Howes et al. 2017). 
• Evidence support for DA hypothesis

  • Curran et al (2004): Amphetamines, which increase DA worsen symptoms in people with schizophrenia and induce symptoms in people without.
  • McCutcheon et al (2020): Post-mortem and live scanning studies have consistently found raised levels of glutamate in several brain regions of people with schizophrenia.
• Contradiction DA Hypothesis

  Tauscher et al (2014): Antipsychotic drugs which reduce DA levels also reduce the intensity of schizophrenic symptoms.