Carlson et al. (2000) Flashcards
what was Carlson’s aim ?
to conduct a literary review to further develop the dopamine hypothesis
what did Carlson hypothesise ?
he believed that glutamate and GABA both play a contributing role in schizophrenia
what is PCP ?
- it is an antagonist of NDMA
- it blocks glutamate from binding to its receptor sites
what is NDMA ?
It is the receptor site for glutamate
where does glutamate come from?
- it lives in the meso-limbic pathway
- it is also present in the meso-cortisol pathway
what does glutamate do ?
- 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
what does hypoglutaminergia trigger?
hyperdopaminergia
what does GABA do ?
- 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
validity of Carlson ?
- analysed secondary data - may not know the quality of the research and may reduce the validity
competing argument of Carlson’s validity ?
- 14/33 of the studies used were his own
- this improves the validity as he knows that his are high quality
objectivity of Carlson ?
- 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
what did Carlson find in relation to schizophrenic medication ?
- 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
give two examples of parkinsonian symptoms ?
- tremors
- shaking
how can Carlson’s findings be applied to schizophrenic medication ?
- 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
why could the new applications improve patient compliance ?
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