Carlsson - contemporary study schizophrenia

Question 1

aim - P1, A01

Answer 1

Carlsson aimed to carry out a literature review of the evidence presented for the dopamine hypothesis and a consideration of other neurotransmitters (Seretonin, glutamate and GABA)

Question 2

method - P1, A01

Answer 2

• 32 studies were included in the review - literature reviews, recreational drug research incluing psychoisis, brain scans, animal research and research using schizophrenic patients and those with parkinsons / huntingdons disease
• the neurotransmitters of interest are dopamine, glutamate and seretonin
• it was a literature review from published studies which have been peer reviewed by other psychologists
• they also looked at brain scans e.g., dopamine receptor activity
• they also looked at studies of recreational drug use such as amphetamines (dopamine antagonist which increases it) and PCP (which is a glutamate antagonist that reduces it) - evidence that both drugs can cause psychosis
• they looked at studies with antipsychotic drugs and animal studies as well

Question 3

strength of method, generalisability - P1, A03

Answer 3

one strength of Carlsson’s study is that there was a wide range of studies included in his review
the literature review was based on animal research, individuals with parkinson, Huntingdon’s and Schizophrenics
this is a wide range of evidence which increases the generalisability of the results to the wider population of schizophrenic patients
therefore, this means that the results found are able to be generalised to the wider population of schizophrenia sufferers due to the bredth of studies used in the review

Question 4

COUNTER ARGUMENT TO strength of method, generalisability - P1, A03

Answer 4

however, some of the studies used in the review were animal studies and rodent research
this means that the research and results may not be applicable to humans with schizophrenia because human expression of the disorder is very different which reduces the generalisability of the study

Question 5

results of the review part 1, what is happening in the meso-cortical pathway - P2, A01

Answer 5

• durgs like PCP and ketamine produced psychotic / schizophrenic symptoms, but instead of activating dopamine, they are antagonists for gluatamate receptorscalled NMDA receptors
• lower glutamate transmission results in reduced dopamine transmission (hypodopaminergia) because although glutamate is an excitatory neurotransmitter, when glutamate levels are low it cannot excite dopamine in the mesocortical pathway. this leads to negative symptoms

Question 6

results of the review part 2, what is happening in the meso-limbic pathway - P2, A01

Answer 6

• hypoglutaminergia in this pathway (blocked NMDA) means that GABA cannot be excited
• GABA is an inhibitory neurotransmitter for dopamine, so cannot do it’s job properly leading to hyperdopaminergia which leads to positive symptoms of schizophrenia

Question 7

results of the review part 3, what is happening in the brain of a schizophrenic - P2, A01

Answer 7

• glutamate acts as an accelerator or brake for dopamine
• if glutamate is faulty it cannot control / regulate dopamine properly
• this leads to either too much or too little dopamine - which causes positive and / or negative symptoms
• dopamine and glutamate pathways work together to ensure that there is not sensory overload by filtering some sensory information to the thalamus (thalamic filter)

Question 10

conclusions - P3, A01

Answer 10

in schizophrenic patients dopamine receptors may be overactive and / or the glutamate is underactive meaning that the thalamic filter does not function properly leading to sensort overloa and the confusion and psychosis seen in schizophrenic patients