Carlsson (2000)

• aim?

  review article aiming to:

  • provide evidence for/against dopamine hypothesis of schiz
  • look beyond dopamine hypothesis at interaction of neurotransmitters including glutamate, GABA, serotonin
  • look at specific brain areas with regard to neurotransmitter interactions
  • use information on psychosis and neurotransmitter functioning to produce new anti-psychotic drugs that are more effective with less side effects
• procedure?

  literature review, so methods and findings of studies to do with neurotransmitter interactions in schizophrenia are analysed. used rodents to test neurotransmitter functioning, studies on people with acute schiz/ schiz in remission, and studies using brain scans that investigate psychosis
• findings on dopamine?

  • PET scans show high levels in dopamine which are related to psychosis. Changes in dopamine levels may be due to some other change in people with schiz, like interactions with other neurotransmitters such as glutamate, GABA, serotonin, acetylchocline.
• findings on glutamate?

  hypoglutaminergia can play a role.

  • Lodge 1989, PCP can induce psychosis by inhibiting action of glutamate in the brain.

  glutamate failure in the cerebral cortex may lead to negative symptoms of schizophrenia, failure in the basal ganglia may lead to positive symptoms.
• findings on the thalamus?

  thalamic filter, thalamus 'filters off' neurotransmitters to stop cerebral cortex from overloading. there are 2 pathways, indirect (too much dopamine/ too little glutamate reduces protective influence) and direct (abnormal dopamine and glutamate cause thalamus to excite and starve cerebral cortex of stimulation)
• findings on serotonin?

  related to dopamine (reduced levels of serotonin= increased dopamine release).

  • clozapine (antipsychotic) reduces both dopamine and serotonin levels in the brain. NMDA antagonists limit glutamate and stimulate serotonin levels
• conclusions for Carlsson?

  • different subpopulations of those with schiz, where schiz is caused by different abnormal levels of different neurotransmitters. implications for treatment
  • glutamate deficiency should be studied and may explain increased dopamine responsiveness.
  • increased serotonin activity is found in people with schiz. both dopamine and serotonin link to pos/neg symptoms.
  • more focus on other neurotransmitters like GABA, acetylchocline is needed
• generalisability?

  • research on animals may not generalise to humans, animal studies cannot investigate role of culture.
  • Luhrmann (2015), differences in auditory hallucinations with people from different cultures.
• reliability?

  • more review articles means clear overview given of topic.
  • wide range of evidence gathered
  • all but one study was peer reviewed
• applications?

  • effective treatments for schiz, both glutamate agonists and serotonin agonists may be effective treatments since they decrease pos/neg symptoms of schiz.
  • review articles mean further research has been set since it can be seen what treatments are best to use
• validity?

  • research uses scientific method, like PET scans. Abi- Dargham (2012) measured dopamine transmission in patients with schiz.
  • however some use scanning to investigate neurotransmitter functioning. since Ps have found it stressful, it may affect their functioning so results may not be valid.
  • secondary data that's analysed is questioned
• evidence?

  • Sendt (2012), glutamate is important in explaining schiz (dopamine on its own doesn't fully explain schiz)
  • Carlsson uses evidence from rodent studies, people with acute schiz/schiz in remission and people with parkinsons
• reductionism?

  • further research on other neurotransmitters is needed, as some interactions are ignored
  • doesn't investigate causes of schiz, like genetics or non-biological factors
  • however it does look into other neurotransmitters and not just the dopamine hypothesis