Carlsson et al (2000)

Question 1

What are the aims?

Answer 1

• To investigate further relationship between levels of neurotransmitter (dopamine and glutamate) on symptoms of schizophrenia through paper review of studies
• To investigate hyperdoperminergia (high dopamine) and hypolutamatergia (low glutamate) as neurochemical explanations

Question 2

What work did Carlsson’s study use?

Answer 2

• Animal studies
• Brain scans
• Carlsson’s own work
• Work of others (e.g. studies of recreational drugs on psychosis)
• Parkinson’s & Huntington’s patients

Question 3

What were the results (PCP & Clozapine)?

Answer 3

• PCP acts as an antagonist for glutamate receptor
• Clozapine is highly effective for schizophrenia as it reduces reported side effects & levels of dopamine and serotonin

Question 4

What were the results (Glutamate failure)?

Answer 4

• Glutamate failure in cerebral cortex led to negative symptoms
• Glutamate failure in basal ganglia lead to positive symptoms

Question 5

What were the conclusions?

Answer 5

• Schizophrenia could have different types which is caused by abnormal levels of different neurotransmitters e.g., GABA
• Further research is needed into developing drugs that treat schizophrenia that avoid negative symptoms

Question 6

What are 2 strengths of Carlsson et al?

Answer 6

• The studies used were laboratory experiments e.g., PET techniques & animal research, which are standardised and replicable, increasing reliability
• Cited 33 studies which is representative of what was going on at the time in his field

Question 7

What are 2 limitations of Carlsson et al?

Answer 7

• Many studies Carlsson cited are animal (particularly mice) experiments which have ethical issues due to them being injected with drugs to bring on psychotic symptoms
• Lots of secondary data used to there’s no way of knowing the reliability or validity of the original study