carlsson et al study

• Carlsson

  Aimed to provide more of an explanation for Sz than simply the dopamine hypothesis. Looked at the relationship between neurotransmitters e.g. dopamine and glutamate and to review antipsychotic drugs that could be more effective with fewer side effects.
• Literature review

  • Conducted on 33 studies (32 published and 1 unpublished)
  • Investigated neurochemical levels in patients diagnosed with schizophrenia and drugs which induce symptoms of psychoses such as PCP
• Studies included in the review

  • Laruelle et al (1996)
  • Miller and Abercrombie (1996)
• Laruelle et al (1996) looked at SPECT and PET studies to measure dopamine release in the basal ganglia. Found that amphetamine challenge enhances this release significantly more in drug naive schizophrenic patients compared to age matched controls, therefore correlating to the induction of schizophrenia symptoms
• Strength of Laruelle et al (1996)

  • High reliability as trained psychologists will always interpret the scan in the same way e.g. red always signifies high activity
  • High validity because there was a large amount of data collected in the 33 studies so any anomalies would have reduced effect and triangulation can occur
• Miller and Abercrombie (1996) found that when imposing an NMDA agonist, the release of dopamine was enhanced
• Strength of Miller and Abercrombie (1996)

  • High generalisability as the literature review included both acute Sz and Sz in remission. Levels of NT's and impact on symptoms can therefore be applied to different experiences of Sz
• Weakness of Miller and Abercrombie (1996)

  • Low generalisability as mice were used to look at the relationship between dopamine and glutamate. Evolutionary discontinuity between rats and humans e.g humans have a more developed PFC and therefore the relationship between dopamine and glutamate in humans may be different
• Carlsson found that PCP leads to psychosis as it acts to block the glutamate receptors and acts as an agonist to decrease the effect of the neurotransmitter, this leads to deficiency in glutamate. This results in cognitive symptoms of schizophrenia such as loss of flexibility and other behavioural issues such as poverty of speech (mainly negative symptoms). Deficiency in the cerebral cortex leads to negative symptoms of schizophrenia.
• Strength of Carlsson's findings

  • High reliability as 33 articles were looked at which all supported the results of each other. For example, Laurelle and Breier both agreed that amphetamines increase dopamine release which in turn leads to positive symptoms of Sz.
• Weakness of Carlsson's findings

  • Low reliability as secondary data is used as it is a literature review of pre-existing studies so we don't know if standardised procedures were followed so we are unable to replicate and test for consistency of findings. Therefore results may not be useful to investigate the role of neurotransmitters to explain Sz.
• Carlsson also found that glutamate regulates dopamine and acts as an accelerator/brake. If there isn't enough dopamine then glutamate will excite the levels and so increase them. However if there is too much dopamine, glutamate can reduce the production of dopamine to reduce the levels. Glutamate acts as an accelerator in the mesocortical pathway (leading to negative symptoms) and as a brake in the mesolimbic pathway, signalling to GABA neurons to inhibit dopamine production (leading to positive symptoms).
• Strength of Carlsson's findings

  • High ethics as one of the aims of the study was to review treatments for Sz and see how they can be improved, therefore it benefits those who were previously treatment resistant and didn't respond to FGA's
• Sendt et al found that we need to do further research into the role of glutamate and therefore this may lead to improvements in treatment and therefore improved quality of life for those with Sz and possibly reintegration to society.