Carlsson Study (Clinical Psychology) Flashcards
When did Carlsson et al’s study take place?
2000
What was the Title of Carlsson et al’s (2000) study?
Network interactions in schizophrenia - therapeutic implications
What was the Aim of Carlsson et al’s (2000) study?
Investigate the role of neurotransmitters on Sz symptoms.
More evidence for dopamine hypothesis.
What 2 camps of neurochemical explanations for schizophrenia did Carlsson et al investigate?
High dopamine Low glutamate
Why did they believe it was important to investigate these 2 views?
This is important to investigate, to try and reduce negative side effects To try to develop drugs that reduce negative side effects with drugs that reduce dopamine
What 3 areas of research did Carlsson et al (2000) review?
- Brain Scans showing link between high dopamine and schizophrenia 2. Recreational Drugs that induce psychosis 3. Research on Drugs that Treat Schizophrenia, and the neurotransmitters of the brain that they effect
What Recreational Drugs did Carlsson look at in his 2000 study?
- amphetamines/speed (increases dopamine, causes hallucinations) 2. PCP/angel dust (reduces glutamate, causes halluncinations).
What were the 3 Key Findings in Carlsson et al’s (2000) study?
Dopamine Hypothesis revisited: PET scan provide evidence for dopamine hypothesis (dopaminergic dysfunction).
- Sz patients > dopamine activity than healthy control group especially in basal ganglia.
Beyond dopamine: neurotransmitters affect each other so is dopamine the only one at play in Sz symptoms? Carlsson focus on glutamate…
- Lodge et al (1989) - glutamate activity at NMDA receptors produces psychotic symptoms in humans and rats.
Glutamatergic control of dopamine release: Glutamate regulates the behaviour of dopamine in the brain - acts as an “accelerator” increasing it or a “brake” decreasing it.
- Miller & Abercrombie (1996) - reduction in glutamate activity leads to an increase release in dopamine (by blocking NMDA receptors which glutamate binds to).
What was the Conclusion of Carlsson et al’s (2000) study?
Carlsson suspects there are “subpopulations” of Sz whos symptoms have different biological explanations.
Lack of glutamate might cause patients to have an exaggerated response to dopamine at post-synapse.
Researchers should start looking into the role of other neurotransmitters e.g. Gaba and acetylcholine.
What are the Strengths of Carlsson et al’s (2000) study?
G: Carlsson et al had combined the finding of many studies in their review meant a large overall sample size R/V: Carlsson used statistical analyses, giving their findings a degree of objectivity, credibility + validity R/V: The brain scans used are standardised and objective methods E: No ethical guidelines were broken
What are the Weakness of Carlsson et al’s (2000) study?
G: Many of the studies reviewed were completed on rats R/V: The validity + reliability of the original data is unknown R: The original data may have been cherry picked
