Contemporary study: Carlson et al (2000) Flashcards
Aim
Conduct evidence for and against the dopamine hypothesis of schizophrenia
Also wanted to explore the glutamate hypothesis
IV, DV and sample
None of this existed as he conducted a meta analysis of 33 studies
Procedure
Meta analysis of multiple studies looking into the role of neurotransmitters in schizophrenia.
- Alot of the studies involved PET scans
Results: The dopamine hypothesis revisited
Evidence for dopamine hypothesis, schizophrenic patients shown to have more dopamine activity than healthy control group.
What part of the brain were these high levels of schizophrenia spotted
Basal Ganglia
Results: beyond dopamine
Carlsson also looked at Glutamate as a possible explanation.
Why did Carlsson look at Glutamate
The drug ‘angel dust’ induced schizophrenic like symptoms and its a powerful antagonist for glutamate receptors.
Results: Glutamate-dopamine interaction at the post synaptic level
Low levels of glutamate link with both positive and negative schizophrenic symptoms
What was the possible cause for positive symptoms
low levels of glutamate in subcortical basal ganglia
What was the possible cause for negative symptoms
Low levels of glutamate in cerebral cortex
Results: Glutamatergic control of dopamine release
Glutamate molecules may release GABA. This causes dopamine activity to decrease. Low levels of glutamate thought to increase dopamine activity.
Results: Comparing 2 experimental schizophrenia models (what were the 2 models)
- Hypodopaminergia
- Hypoglutamatergia
What is hypodopaminergia
low levels of dopamine
What is hypoglutamatergia
low levels of glutamate
What did Carlsson find when comparing these 2 models
These 2 models can explain why some people respond better to some antipsychotics than others.
- Some people who dont respond typical antipsychotic
drugs that reduce dopamine might have a more
glutamatergic condition instead