Carlsson et al (1999) Flashcards

1
Q

Aims?

A
  • 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
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2
Q

Procedure?

A
  • 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
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3
Q

What were the 4 parts to the results of Carlsson’s study?

A

1) Dopamine as an explanation for schizophrenia
2) Glutamate as an explanation for schizophrenia
3) Glutamate and dopamine interaction
4) Drug treatments

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4
Q

Briefly describe the first part of the results

A

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

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5
Q

Briefly describe the second part of the results

A

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

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6
Q

Briefly describe the third part of the results

A

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

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7
Q

Briefly describe the fourth part of the results

A

4) Drug treatments

- Clozapine is highly effective with less side effects

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8
Q

Conclusions?

A
  • 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
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9
Q

Strength?

A

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

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10
Q

Weakness?

A

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

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11
Q

Strength?

A

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

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12
Q

Weakness?

A

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

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