Carlson et al. (2000) Flashcards

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1
Q

what was Carlson’s aim ?

A

to conduct a literary review to further develop the dopamine hypothesis

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2
Q

what did Carlson hypothesise ?

A

he believed that glutamate and GABA both play a contributing role in schizophrenia

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3
Q

what is PCP ?

A
  • it is an antagonist of NDMA

- it blocks glutamate from binding to its receptor sites

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4
Q

what is NDMA ?

A

It is the receptor site for glutamate

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5
Q

where does glutamate come from?

A
  • it lives in the meso-limbic pathway

- it is also present in the meso-cortisol pathway

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6
Q

what does glutamate do ?

A
  • glutamate’s job is to control other neurotransmitters
  • it tries to break down dopamine to slow down its uptake
  • in the meso-cortisol pathway, dopamine is slower and so glutamate has to speed it up
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7
Q

what does hypoglutaminergia trigger?

A

hyperdopaminergia

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8
Q

what does GABA do ?

A
  • it helps glutamate reign in dopamine if there is too much of it
  • sometimes there is a signal failure though and GABA doesn’t receive glutamate’s message for help
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9
Q

validity of Carlson ?

A
  • analysed secondary data - may not know the quality of the research and may reduce the validity
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10
Q

competing argument of Carlson’s validity ?

A
  • 14/33 of the studies used were his own

- this improves the validity as he knows that his are high quality

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11
Q

objectivity of Carlson ?

A
  • the research that he analysed had used SPECT and PET Scans
  • by using scientific technology, it makes the results more objective
  • this is because there is no researcher bias
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12
Q

what did Carlson find in relation to schizophrenic medication ?

A
  • schizophrenic patients in remission would complain of parkinsonian symptoms - which was a result of the drugs they were taking that reduce dopamine
  • Carlson found that low levels of glutamate trigger higher levels of dopamine
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13
Q

give two examples of parkinsonian symptoms ?

A
  • tremors

- shaking

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14
Q

how can Carlson’s findings be applied to schizophrenic medication ?

A
  • shifting focus from dopamine to glutamate and GABA
  • e.g., drugs that focus on pre-synaptic neuron rather than post-synaptic neuron so that levels of dopamine can be controlled without causing hypodopaminergia
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15
Q

why could the new applications improve patient compliance ?

A

if the new drugs do not cause parkinsonian symptoms then patients will be more likely to take them, as the side-effects will not be as bad

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