Carlsson et al (1999) Flashcards
Aims?
- To review studies that show the relationship between SZ and dopaminergic dysfunction
- To explore glutamatergic deficiency
- To use their understanding to produce a new anti-psychotic drug that has fewer side effects
Procedure?
- Conducted a meta-analysis, using 32 pieces of previous research
- Completed a literature review
- The previous research that was analysed came from a range of areas - using animals, SZ’s and patients with Parkinson’s/Huntington’s (PET scans)
- The animal research was used to show the impact of recreational drugs on reducing glutamate levels in the brain to show SZ like symptoms
What were the 4 parts to the results of Carlsson’s study?
1) Dopamine as an explanation for schizophrenia
2) Glutamate as an explanation for schizophrenia
3) Glutamate and dopamine interaction
4) Drug treatments
Briefly describe the first part of the results
1) Dopamine as an explanation for schizophrenia
- SZ patients showed more dopamine activity than a healthy control group, especially in basal ganglia
- However, Laruelle et al found that SZ patients in remission had normal dopamine activity - suggests that high dopamine levels were a symptom of SZ and not a cause
Briefly describe the second part of the results
2) Glutamate as an explanation for schizophrenia
- PCP acts as a glutamate antagonist, blocking glutamate receptors
- PCP leads to psychosis
- Questions whether glutamate deficiency has a role in psychosis
- Glutamate failure in cerebral cortex = negative symptoms
- Glutamate failure in basal ganglia = positive symptoms
Briefly describe the third part of the results
3) Glutamate and dopamine interaction
- Dopamine receptors are affected by glutamatergic neurons acting as accelerators/brakes
- Glutamate and dopamine interact; reduced glutamate functioning = increased dopamine release
Briefly describe the fourth part of the results
4) Drug treatments
- Clozapine is highly effective with less side effects
Conclusions?
- Carlsson suspects there a probably different groups of SZ patients whose symptoms have different biological explanations
- Researchers should start looking at other neurotransmitters, like GABA and acetylcholine
Strength?
P- Reliable
E- The studies cited are all lab experiments, which use PET scans
E- These techniques are standardised and replicable, making the research reliable
Weakness?
P- Unreliable
E- Reliance on secondary data from a variety of sources
E- There is no way of knowing how reliable the original studies were. Therefore, basing conclusions about treatments on this research could be problematic
Strength?
P- Valid
E - Use of secondary data allowed a great deal of research to be brought together quickly, providing an overview. The research is from a range of areas - animal studies, SZ’s and patients with Parkinson’s/Huntington’s
E- This mass information allows for more valid conclusions to be drawn and gives depth
Weakness?
P- Invalid
E- Previous studies used animals. Human behaviour and response to drugs would be much more complex than animals, despite sharing similar brain structures
E- Studies may lack generalisability and therefore reduces the credibility of the study based on the chosen secondary research