Contemporary study: Carlson et al (2000) Flashcards

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1
Q

Aim

A

Conduct evidence for and against the dopamine hypothesis of schizophrenia

Also wanted to explore the glutamate hypothesis

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2
Q

IV, DV and sample

A

None of this existed as he conducted a meta analysis of 33 studies

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3
Q

Procedure

A

Meta analysis of multiple studies looking into the role of neurotransmitters in schizophrenia.

  • Alot of the studies involved PET scans
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4
Q

Results: The dopamine hypothesis revisited

A

Evidence for dopamine hypothesis, schizophrenic patients shown to have more dopamine activity than healthy control group.

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5
Q

What part of the brain were these high levels of schizophrenia spotted

A

Basal Ganglia

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6
Q

Results: beyond dopamine

A

Carlsson also looked at Glutamate as a possible explanation.

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7
Q

Why did Carlsson look at Glutamate

A

The drug ‘angel dust’ induced schizophrenic like symptoms and its a powerful antagonist for glutamate receptors.

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8
Q

Results: Glutamate-dopamine interaction at the post synaptic level

A

Low levels of glutamate link with both positive and negative schizophrenic symptoms

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9
Q

What was the possible cause for positive symptoms

A

low levels of glutamate in subcortical basal ganglia

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10
Q

What was the possible cause for negative symptoms

A

Low levels of glutamate in cerebral cortex

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11
Q

Results: Glutamatergic control of dopamine release

A

Glutamate molecules may release GABA. This causes dopamine activity to decrease. Low levels of glutamate thought to increase dopamine activity.

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12
Q

Results: Comparing 2 experimental schizophrenia models (what were the 2 models)

A
  1. Hypodopaminergia
  2. Hypoglutamatergia
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13
Q

What is hypodopaminergia

A

low levels of dopamine

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14
Q

What is hypoglutamatergia

A

low levels of glutamate

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15
Q

What did Carlsson find when comparing these 2 models

A

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
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16
Q

Conclusion: what did Carlsson conclude

A

There are probably different groupd of schizophrenia patients whos symtoms have different explanations. There fore more research needs to be done on other neurotransmitters

17
Q

EVALUATION

A

Evaluation

18
Q

What is a strength of the generalisability

A

The studies that were reviewed are very representative selection of what was going on at the time of the field

19
Q

Why would the studies be very representative

A

Carlsson was a top researcher into dopamine aswell as schizophrenia, he even won a nobel prize.

20
Q

What is a weakness of the generalisability

A

Study is time locked

21
Q

Why is this study time locked

A

it was conducted in 2000, so it cannot be representative of what we know now.

22
Q

What is a strength of the reliability

A

All the studies carlsson looked at are easy to replicate

23
Q

Why are the studies carlsson looked at easy to replicate

A

They were lab experimentas that used modern brain imaging techniques like PET scans

24
Q

What is a strength of the application of Carlssons analysis

A

It led to the improvements of drug treatments based on new understanding of neurotransmitter pathways

25
Q

What are some improvents of drug treatment it caused

A

new dopaminergic drugs now are more effective with fewer side effects
- new atypical drugs now effect more neurotransmitters like Glutamate and serotonin

26
Q

What is a weakness of the validity of the meta analysis

A

The results were gathered through secondary data and most of the studies he looked at were lab experiments

27
Q

How does secondary data affect the validity

A

You wouldn’t know if the participants were acting normally in a realistic setting. In this case most likely not because most the studies were lab experiments.