Carlsson

Carlsson wanted to review studies to research the relationship between different NTs (especially dopamine and glutamate) on the symptoms of sz. Also considering rival theories such as glutamatergic deficiency

representative - used sz patients in remission, acute episodes, pos + beg symptoms and treatment resistent patients.
increased generalisability

G:
-> animal data - gave amphetamines to rodents, where they reported symptoms such as hallucinations
-> W: anthropomorphic assumption as we cannot confirm they did. and humans have more complex cognitive functioning + different environmental factors
-> this means that Carlsson's findings aren't generalisable to the human population as the data cannot reflect NT functioning in humans

-> standardised procedure. carlsson carried out a literature review which is secondary data, that used animal studies, postmortems, brain scans and human ppt research
-> Laurelle gave sz ppts in acute episodes, an amphetamine induced release dopamine.
-> Miller + Abercrombie (1996) used rodents to test NT levels where competitive NMDA inhibibited dopamine release.
-> therefore, standardised procedure that makes it easy to replicate the study to check for consistency of findings of NTs and sz

-> literature review means secondary data. cannot be sure of sound methodology and level of control over extraneous variables
-> therefore Carlsson's findings may be invalid, affected by factors such as ecological validity as the studies Carlsson reviews are lab experiments meaning NT activity may be unreflective of real life situations.

-> objective quantitative data. PET scans revealed sz patients had increased dopamine activity when compared to healthy controls, when measuring the basal ganglia. And Laurelle et al found sz patients in remission were within the normal range. Miller and Abercrombie found when inhibiting NMDA with antagonists, it allows dopamine levels to rise due to decreased glutamate - this suggests high glutamate activity inhibits dopamine.
-> increased internal V, objective, quantitative, easy to find cause and effect between NTs and sz.

- reviewed 33 studies where 14 were his own
- lowers internal V because he knows his studies will support his hypothesis that sz is caused by different NTs

-> improving drug treatment because he found clozapine is an SGA, which binds to dopamine and serotonin.
-> However, it is one of the weakest dopamine antagonists which suggests new treatments need to be made that don't solely focus on dopamine.
-> therefore, this could improve conditions for the 15% of sz patients who are non-responsive to current sz treatment

- brief overview
- sample increased gen
- animal data decreased gen
- reliability increased
- secondary data decreased val
- objective quan data
- publication bias
- application drug treatments