Carlsson (1999)

Question 1

Aims

Answer 1

1. To use what is known about NT function and psychosis to provide more of an explanation for Sz than simply the dopamine hypothesis
2. To consider the need for further research into drug treatments that target NTs other than dopamine and improve drug treatments by reducing relapse rates as well as side effects
3. To use understanding of psychosis and links to NT functioning to produce new anti-psychotic drugs that could be more effective with fewer side effects

Question 2

Research method

Answer 2

meta-analysis

Question 3

Procedure

Answer 3

Many previous studies have linked amphetamines (increase dopamine) with Sz
There is other research linking the use of PCP with psychosis
The researchers also draw on evidence from studies into the effectiveness of drugs used to treat Sz and the method of action they have on the brain to support the hypothesis that there may be other NTs associated with Sz
Findings from studies such as:
* previous research using rodents to test NT functioning and related brain structure
* studies with acute Sz and Sz in remission
* evidence from looking at mice

Question 4

Results: General

Answer 4

Excess dopamine is likely to be too simplistic as a cause, as it is unlikely to be the only dysfunctional NT in Sz

The review lists noradrenaline, serotonin, acetylcholine, glutamate and GABA as the NTs likely to relate to Sz - dopamine is easier to study in the live brain