Carlsson Questions

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  • Created by: mimipopx
  • Created on: 08-10-16 10:06
Carlsson et al use the terms agonist and antagonistwithin their review. What do these terms mean?
Agonist- activates the receptor at the site of the receptor so a message is passed on and so increased activity. Antagonist- blocks the receptor at the site of the receptor and deactivates it= decreasing activity.
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What types of methodology were used in the studies that were reviwed?
Brain scans and animal studies
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What type of glutamate receptors does PCP have an efect on? An what result does this have on behaviour?
NMDA receptors. It results in psychosis
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Why is it thought that serotonin could also be involved in schisphrenia?
Because clozapine is given as a treatment and this reduces dopamine and serotnin activity.
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What explanation os given by carlsson as to how glutamate and dopamine can lead to psychosis?
Thalamic filter explanation- NTs work in pathwaysto filter out sensory info so we are not overloaded. I this does nothappen , it may lead to senspry overload which results in psychosis.
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What was the key conclusion that Carlsson made about the drugs that are used to treat schizophrenia?
Further reseach needs to be conducted into developing drugs to treat schizophrenia that avoid negative side effects, considering the role of other NTs.
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What do the terms hyp and hyper mean?
Hyper= too much, Hypo= too little
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Before this review what were the two main camps of thought that existed about schozophrenia?
That it was either caused by high levels of dopamine or low levels of glutmate.
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What hypothesis was made about the cause of schizophrenia?
That other neurotransmitters, other than dopamine, may be invloved in the development of the disorder
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What does it mean to say that glutamate acts an accelerator or brake to dopamine?
The actvity of the NTs are related- glutamate can influence dopmaine activityby increasing or reducing it.
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Why is there a problem in studying the role of glutamate?
Glutamate has a role in cell metabolism as well as a neurotransmitterso it is hard to measure glutamate release
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What is the overall suggestion made about the cause of schizophrenia in relation to dopamine and glutamate?
That low levels of glutamate may impact upon the levels of dopamine - creating excess levels and activity.
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What does animal research with NMDA antagonists suggest?
animal research with NMDA antagonists can stop dopmaine release, sop it seems dopamine and glutamate are not the only NTs involved.
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What types of methodology were used in the studies that were reviwed?

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Brain scans and animal studies

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What type of glutamate receptors does PCP have an efect on? An what result does this have on behaviour?

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Card 4

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Why is it thought that serotonin could also be involved in schisphrenia?

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Card 5

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What explanation os given by carlsson as to how glutamate and dopamine can lead to psychosis?

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