Contemporary Carlsson 2000 Flashcards
(9 cards)
aim of carlsson 2000
explored relationship between SZ, dopaminergic dysfunction and hypoglutamatergia, to conduct further research into drug treatments/side effects
to test the validity of his dopamine hypothesis and the rival glutamate hypothesis, did this by conducting a literature review of 33 studies on NTs
sample of carlsson 2000
literature review of 33 studies with 1 unpublished
Carlsson primarily conducted 14 of the 33 studies
all the studies that were used focused on acute episodes of SZ, can be argued that these examples of acute episodes can be used as an indicator for the symptoms of SZ
carlsson 2000 - lindstroem
L-DOPA study
found increased dopamine receptors in the brains of SZs in post-mortem studies using PET scans
supports his review in studying his dopamine hypothesis- the idea that SZ have more D2 receptors, so more dopamine binding and dopamine uptake causing positive symptoms such as hallucinations/delusions. Carlsson theorised that hyperdopaminergia in mesolimbic pathway causes these positive symptoms, and dysfunction of dopamine in the mesocortical region causes negative symptoms such as flatness of emotions/apathy/social withdrawal
scientific evidence using PET scans increases the credibility of his theory as a result.
carlsson 2000 - laruelle
amphetamines act as dopamine agonists, leading to higher release of dopamine in SZ using PET scans
use of PET scans is a strength as objective evidence increases validity
PET scans can create stress for the individual, which changes brain activity due to altered NT functioning under stress and so the study may not measure normal levels, reducing validity
carlsson 2000 - glutamate hypothesis
the idea that glutamate acts as an accelerator or brake for dopamine
discusses that glutamate failure in the basal ganglia causes positive symptoms, while glutamate failure in cerebral cortex causes negative symptoms
however, some of the research he used may be time-locked, as research has advanced to include other NTs so some conclusions may no longer be valid
carlsson 2000 - lodge et al
glutamate hypothesis is supported by lodge et al, who found that NMDA antagonists such as PCP are psychostimulants in rodents, mimicking symptoms of psychosis in humans
this may be generalisable to humans as we can assume that we share similar biological brain and hormonal functions to rodents, but we’re inferring SZ symptoms from behaviour so if inferences are wrong it may not be reliable due to subjectivity
carlsson 2000 - miller and abercrombie
supports the glutamate hypothesis as they used animal studies of rodents to view how NMDA antagonists increased release of dopamine
animal studies conducted in lab environments with strict controls meant that there were no extraneous variables, so we can be confident that NT levels change because of antagonist, meaning that the causal relationship increases validity
however, the use of secondary data means Carlsson didn’t conduct all the studies himself, so research may not be directly related to aims of study or accurately created as he couldn’t directly manipulate or control variables, decreasing validity as a result
carlsson 2000 - thalamic filter
idea that NTs are filtered off to prevent cerebral cortex overload
said that the indirect pathway is hyperdopaminergic & hypoglutamatergic so reduce protective influence of thalamus and cause positive symptoms, while the direct pathway means abnormal D/G levels excite the thalamus & understimulate the cerebral cortex, causing negative symptoms
all this research was made accessible on public domain for other people to review and provide validate conclusions, therefore providing the research with inter-rater reliability, yet there may be publication bias on explanations as only research with significant outcomes more likely to be published, decreasing validity
conclusions of carlsson 2000
the dopamine theory alone was too reductionist, simple and needs to be paired with more research into glutamate, serotonin and GABA
Sendt et al confirms that drugs only linked to dopamine are ineffective, so Carlsson claims that we must develop drug treatments with reduced side effects, maybe even 3rd generation
