dopamine hypothesis

• INITIAL EXPLANATION

  most common, works on basis that we use drugs to treat, does it describe the process / cause

  +ve symptoms = due - high levels of dopamine

  dopamine neurons play a key role in attention + any disturbances > problems with functions: attention, perception and thoughts (-ve)

  this is based on research that induced psychosis (Sz like symptoms) through administering amphetamines (act as dop agonist)

  suggests that dop agonists > psychosis symptoms
• REVISED HYPOTHESIS

  • technology and research - advanced > discovered different subtypes of dopamine receptor sites in different areas of the brain (D1-D4) e.g. cerebral cortex and limbic system
  • more modern research shows - AP drugs affect D2 receptors and block (mainly in MLP) and reduce positive symptoms > revised hypothesis > in depth understanding of ROD in brain and in relation to SZ symptoms
  • doesn't explain negative symptoms
• ROLE OF DOPAMINE IN LOCALISED BRAIN AREAS - Mesolimbic Pathway (also occurs in Nigrostriatal Pathway)

  > Hyperfunction in D2 activity > positive symptoms

  signals - VTA > NA (D2 receptors located)

  too much dopamine (hyperfunction) from neurons firing too quickly / too often > overstimulation of receptors > positive symptoms

  > supported by AP > reducing dopamine transmission and activity > reduce positive symptoms
• ROLE OF DOPAMINE IN LOCALISED BRAIN AREAS - Mesocortical Pathway

  > Hypofunction of D1 activity > negative symptoms

  signals - VTA > PFC /FL (D1 receptors located)

  too little dopamine (hypofunction) in this brain area > associated with people who have Sz symptoms (-ve) and cognitive impairments + processes slow down and normal functioning > mixed

  MCP - vital in emotional responses, motivation, movement and cognition

  unable to treat