Contemporary study: Carlson et al (2000) Flashcards

(27 cards)

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

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
What are some improvents of drug treatment it caused
new dopaminergic drugs now are more effective with fewer side effects - new atypical drugs now effect more neurotransmitters like Glutamate and serotonin
26
What is a weakness of the validity of the meta analysis
The results were gathered through secondary data and most of the studies he looked at were lab experiments
27
How does secondary data affect the validity
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.