Carlsson et al

Question 1

What were the aims of the study?

Answer 1

• The aim is to present the current view of the relationship between schizophrenia and dopaminergic dysfunction
• Another aim is to explore a rival theory, that a glutamergic deficiency or hypoglutamergia.

Question 2

What was the sample like?

Answer 2

• A literature review was done.
• Carlsson et al not carrying out empirical research and they do not have a sample of their own.
• However, they refer to a number of earlier studies that do not have samples of patients with schizophrenia

Question 3

What was the Procedure like?

Answer 3

• No procedure however, they refer to a number of earlier studies that use PET.
• PET scans is a brain imaging technique which injects the participants with a radioactive tracer that dissolves in the blood stream
• A PET scan detects the radioactivity and converts it into a digital image of the brain, highlighting the active areas in yellow and red.
• Glutamate - dopamine interaction at the post synaptic level
• low levels of glutamate seems to link with both positive and negative symptoms
• Basal Ganglia - brain reward centre -> positive symptoms
• low glutamate activity in the cerebral cortex -> negative symptoms

Question 4

What were the results - Dopamine Hypothesis Revisited?

Answer 4

• Schizophrenic participants show more dopamine activity than a healthy control
• Laurelle et al (1999) - found that schizophrenia patients in remissionely had normal dopamine activity
• patients taking anti-psychotics complain most about the side-effects

Question 5

What were the results - BEYOND DOPAMINE?

Answer 5

• Drugs like pcp and ketamine produces antipsychotic symptoms
• Lodge et al (1989) - claim glutamate activity at NMDA receptors produces reduction in rats and humans

Question 6

What were the results - GLUTAMATERGIC CONTROL OF DOPAMINE RELEASE?

Answer 6

• Glutamate seems to regulate the behaviour of dopamine and sheds some light on the behaviour of dopamine in the brain.
• Miller and Abercombine (1996) showed that release of dopamine increased if glutamate activity is reduced.

Question 7

RESULTS - THALAMIC FILTER?

Answer 7

• Carlsson proposed that the thalamus filters of neurotransmitters coming out of the statrium to stop the cerebral cortex from overflowing.
• INDIRECT PATHWAY - too much dopamine, too little gluatamate reduces protective influence of thalamus.
• DIRECT PATHWAY - abnormal dopamine and glutamate activity excites thalamus.

Question 8

RESULTS - TWO EXPERIMENTAL MODELS

Answer 8

• Some patients respond to some drugs better than others (dopaminergic and glutamergic)
• treatment patients do not respond to typical antipsychotics - have a glutamate condition

Question 9

RESULTS - IS THE THERAPEUTIC POTENTIAL OF DOPAMINERGIC AGENTS EXHAUSTED?

Answer 9

• Carlsson researching new drugs which regulated dopamine activity without producing harmful hypodopamergia
• work by activity at the pre-synapse rather than post synpase
• drugs are now in clinical trails

Question 10

CONCLUSIONS

Answer 10

• Carlsson suspected there are probably different groups of schizoprenia patients whose symptoms have different biological explanation
• lack of glutamate might cause patients to have an exaggerate response to dopamine at the post-synpase