neurotransmitters

• hypothesis?

  schiz can be explained by changes of dopamine functioning in brain
• excess dopamine? (hyperdopaminergia)

  explains pos symptoms due to activity in mesolimbic pathway

  • high levels of dopamine, can be due to low levels of enzyme beta hydroxylase which breaks down dopamine so build up is seen.
  • excess numbers of dopamine receptors, Owen (1978), post mortem examinations of brains show a higher density of dopamine receptors in cerebral cortex of those who suffer with schiz.
  • hypersensetivity of dopamine receptors (D2), overreacting to presence of dopamine
• dopamine deficiency? (hypodopaminergia)

  explains neg symptoms by activity in mesocortical pathway.

  • irregular serotonin activity- serotonin regulates dopamine
• evidence for neutotransmitter evaluation?

  many drugs do work by blocking dopamine but not all people respond to it.

  • Alpert and Friedhoff (1980), some patients didn't improve at all after taking dopamine antagonists.
  • Zipursky (2007), review article showing PET scans can e used to show extent meds block dopamine receptors. It doesn't always remove symptoms in patients who have schiz for 10 years or more even if block is 90% effective.
  • other drugs like clozapine are effective but block neurotransmitters other than dopamine.
• individual differences in neurotransmitter evaluation?

  people with schiz are more sensitive to dopamine uptake, scanning shows those with schiz are more sensitive to excess dopamine than other people (Carlsson 2000) since those with schiz given amphetamines have a greater release of dop than those with no schiz.

  • however amphetamines produce only symptoms similar to pos symptoms of schiz, dopamine hypothesis isn't sufficient explanation as it doesn't account negative symptoms
• applications for neurotransmitter evaluation?

  • people given a drug for Parkinsons disease that increases dopamine production will experience schiz-like symptoms, showing testable evidence for how dopamine plays a role.
  • glutamate also plays a role (psychotic symptoms if blocked, shown in those who take PCP so dopamine isn't only neurotransmitter.
  • we cannot prove excess dopamine causes schiz but is just a symptom
• reductionism in neurotransmitter evaluation?

  explains both pos and neg symptoms of schiz, other explanations struggle to explain neg symptoms. seen where increase of dopamine in mesolimbic pathway= pos symptoms, decrease in mesocortical= neg symptoms.

  • reductionist, focuses purely on neurotransmitter roles, ignoring any other biological or social factors. Brown and Birley (1968), 50% schiz patients report a major life event in 3 weeks prior to relapse showing social conditions can trigger relapse