Sz Contemporary Study - Carlsson et al. (2000)

Question 1

What were the 2 aims of Carlsson et al (2000)?

Answer 1

To review the literature on:
+ The relationship between Sz and hyper-dopaminergic dysfunction
+ Hypo-glutamatergic dysfunction as a rival explanation

To use new insight/ knowledge gained of psychosis and neurotransmitter functioning, to produce new anti-psychotic medication with fewer side effects

Question 2

What were the methodology and sample of Carlsson et al (2000)?

Answer 2

Methodology: Literature review

Sample:
+ Does not have its own sample
+ Reviews previous studies

Question 3

What was the procedure of Carlsson et al (2000)? (3 points)

Answer 3

They conducted a literature review of 32 studies involving mice and human Sz patients exposed to different drug therapies and PET/SPECT scans

Used a triangulated approach in his literature review, which was funded by the Theodore & Vanda Stanley Foundation

No IV or DV in Carlsson’s study - not empirical research as they did not collect their own data

Question 4

What were the 3 main findings of Carlsson et al (2000)?

Answer 4

1. The Dopamine Hypothesis Revisited
2. Beyond Dopamine
3. Glutamergic control of dopamine release

Question 5

What is Carlsson’s first finding ‘The Dopamine Hypothesis Revisited’ and what are its supporting and refuting pieces of evidence? (4 points)

Answer 5

Sz being caused by increased dopamine

Supporting:
Hietala et al (1994):
PET scans showed increased dopamine in Sz patients’ basal ganglias compared to control group

Laruelle et al (1996):
Increased dopamine release correlated with positive symptoms of Sz

Refuting:
Correlation doesn’t mean causation - might only be a ‘subpopulation’ of Sz patients with dopamine dysfunction

Question 6

What is Carlsson’s second finding ‘Beyond Dopamine’ and what is its supporting piece of evidence? (3 points)

Answer 6

Unlikely that dopamine is the only neurotransmitter involved in Sz - others might be involved like:
+ Noradrenaline
+ Serotonin
+ Acetylcholine
+ Glutamate
+ GABA

Supported by: Laurelle et al (1996)
+ Glutamate NMDA receptor antagonist Ketamine and PCP ‘angel dust’ caused an increase in amphetamine-induced dopamine release in humans
+ Suggests that glutamate is involved

Question 7

What is Carlsson’s third finding ‘Glutamergic control of dopamine release’ and what are its supporting and refuting pieces of evidence? (3 points)

Answer 7

Describes how Glutamate acts as an “accelerator” or a “brake” for regulating dopamine activity

Supported by: Miller & Abercrombie (1996)

Refuted by: Martin et al (1998)

Question 8

How does Miller & Abercrombie (1996) support the glutamatergic control of dopamine release? (2 points)

Answer 8

Treated awake rats with MK-801, a glutamate NMDA antagonist

Caused increased release of dopamine - suggests a regulatory relationship between dopamine and glutamate

Question 9

How does Martin et al (1998) refute the glutamatergic control of dopamine release? (2 points)

Answer 9

M100907 antagonist that selectively inhibits 5-HT2A receptor in rats caused a decrease in behavioural abnormalities and psychosis

Suggests the need for a new clinical therapy for paranoid Sz patients using serotonin antagonists rather than of glutamate and dopamine

Question 10

What was the conclusion for Carlsson et al (2000)? (3 points)

Answer 10

A relationship between glutamate deficiency and increase in dopamine is indicated

Subpopulations of Sz exist who may have different causes of Sz not linked to dopamine and glutamate activity

Other neurotransmitters need further investigation for new clinical therapy targets like:
+ Serotonin
+ Acetylcholine
+ GABA
+ Neuropeptides

Question 11

How generalisable is Carlsson et al (2000)? (4 points)

Answer 11

Low generalisability - this was not empirical research so did not involve obtaining primary data

Secondary data was read and reviewed by Carlsson linking neurotransmitters like Dopamine and Glutamate to symptoms of Sz in both mice and humans

Rats are not representative of humans - their CNS and brain anatomy are less complex than that of humans, who exhibit:
+ Higher cognitive functioning
+ Motivation
+ Consciousness of behaviour

Therefore, the results of Carlsson’s study cannot be directly generalised to human Sz patients

Question 12

How reliable is Carlsson et al (2000)? (3 points)

Answer 12

Carlsson’s study can be considered reliable as other researchers could repeat the same literature review process to test for inter-rater reliability

Carlsson examined a range of studies and methodologies on the role of neurotransmitters in Sz - no one method or research study alone led to the conclusions made

This establishes greater credibility in the results

Question 13

How applicable to real life is Carlsson et al (2000)? (3 points)

Answer 13

Its findings have strong application for Sz patients in real-life settings

The finding from ‘Martin et al’ suggests the need for a new clinical therapy which targets serotonin receptors instead of glutamate and dopamine-targeting medications

This could lead to new treatments being provided for Sz patient subpopulations

Question 14

How internally valid was Carlsson et al (2000)? (5 points)

Answer 14

Criticised for a lack of transparency during the peer review process

Subject to researcher bias - Carlsson has not specified the selection criteria used for the inclusion of studies

Carlsson cites one of his sources for SPECT scanning as ‘(Laruelle et al, personal communication)’ - was unpublished at the time

11 of the 32 studies reviewed by Carlsson were his own

Difficult to establish cause and effect between neurotransmitter functioning and Sz due to questionable credibility of studies cited

Question 15

How ethical is Carlsson et al (2000)?

Answer 15

Literature reviews do not involve primary data collection of selection of participants - we can assume BPS ethics were followed