biological explanation for SZ - neurotransmitters

• dopamine

  • too many dopamine receptor sites in brain = too much dopamine being used which leads to symptoms of SZ
  • as dopamine receptors are concentrated around the reward pathway = overactivity in this area causing symptoms like hallucinations and delusions
  • SZ have higher numbers of D2 receptor sites = more likely to pick up dopamine than other sites
• too much dopamine in mesolimbic pathway

  causes positive symptoms of SZ such as delusions
• too much dopamine in neocortical system

  causes negative symptoms of SZ such as disorganised speech
• glutamate

  • a decrease in glutamate cause symptoms like psychosis
  • controls amount of dopamine released by the brain and lowers levels of dopamine
  • decreased glutamate = increased amount of dopamine released
• strength

  • medication targeting dopamine is effective
  • antipsychotic drugs work by blocking dopamine receptors so preventing dopamine continuing to act on neural pathways which is effective in reducing SZ symptoms
  • suggests dopamine is likely to be a major cause of SZ so increasing credibility of dopamine hypothesis
• weakness

  • research evidence suggests 1/3 of patients with SZ don't respond to treatment
  • alpert and freidhoff (1980) found some patients show no improvement in symptoms when taking typical dopamine agonists
  • suggests that dopamine is not the cause of symptoms and other factors must contribute to SZ
• strength

  • evidence to suggest dopamine is metabolised differently in schizophrenics compared to controls
  • lindstroem et al (1999) found schizophrenics who were given L-DOPA used it faster than control group suggesting they were used to producing more dopamine at a quicker rate
  • suggests those with SZ are more sensitive to dopamine than other people so dopamine has crucial role in SZ
• weakness

  • research evidence to suggests that increased dopamine levels do not create symptoms of SZ
  • depatie & lal (2001) found giving people drugs to increase production of dopamine does not create symptoms of SZ as would be expected if excess dopamine caused it
  • therefore, dopamine hypothesis cannot be the only explanation for what causes SZ