Dopamine hypothesis

• Initial dopamine hypothesis

  Brains of SZ patients produce more dopamine than normal brains (hyper-dopaminergia).

  This was found when patients with Parkinsons disease showed SZ-like symptoms when they took a medication that increased the amount of dopamine in the brain.

  However, this explanation was found to be too simple as treatments that lowered dopamine levels reduced positive symptoms but not negative.
• Revised dopamine hypothesis

  Over activity of the mesolimbic pathway (ventral tegmental area to nucleus accumbens) leads to positive symptoms.

  Mesocortical pathway dysfunction (hypodopaminergia) (ventral tegmental area to the frontal lobe) leads to negative and cognitive symptoms of SZ.
• Falkai et al

  Autopsies have found that people with SZ have a larger than usual number of dopamine receptors.

  Excess of dopamine found in left amygdala.

  Concluded that dopamine production is abnormal for SZ compared to normal controls.
• Parkinson’s disease research

  L-Dopa raises dopamine activity in the brain, reducing Parkinsonian symptoms.

  Patients began to develop SZ symptoms.
• Lindstroem et al

  L-Dopa (dopamine releasing drug) was administered to 10 patients with SZ and 10 with no diagnosis of SZ.

  L-Dopa stays in the brain of SZ patients for longer - synapses did not absorb it because the D2 receptors inhibited transmission.

  Suggests this is why SZ patients have excess levels of dopamine. They have more dopamine receptors.
• Antipsychotics

  Target the release of neurotransmitters at the synapse.

  Block the transmission of dopamine on the postsynaptic neuron which leads to a reduction in neural activity.

  This then leads to a reduction in positive symptoms.
• Strengths of the dopamine hypothesis

  Scientific (brain scans)

  Objective - validity

  Supporting evidence

  Deterministic

  Reductionist

  Gives way to biological treatments
• Weaknesses of dopamine hypothesis

  Ignores nurture influences

  Deterministic

  Reductionist

  Critique evidence (eg post-mortem research may not reflect live brains).