Biological Factors

Question 1

First Version - Carlson and Lindquist 1957

Answer 1

• identified that these drugs reduced dopamine uptake level when used on animals
• high numbers of D2 receptors on receiving neurons which lead to more dopamine binding and neuron firing
• evidence from schizophrenic patients have high D2 receptor numbers
• disturbances in dopamine neurons could lead to problems of attention, perception and thought

Question 2

Second Version - Davis 1991

Answer 2

• contradicts version 1
• evidence that dopamine receptors show different brain distribution
• negative symptoms come from the prefrontal hypodopaminergia
• positive symptoms come from striatal hyperdopaminergia

Question 3

Third Version - Howes and Kapur 2009

Answer 3

• links risk factors to increased presynaptic striatal dopaminergic functions rather than D2 receptor activity
• dopamine dysregulation linked to psychosis rather than schizophrenia

Question 4

Caspi et al (2008)

Answer 4

• Majority think that cannabis has minimal levels of harm, however 25% of the population have a val/val variant which is a version of the COMT gene that leads to over reactivity of the enzyme meaning that they are prone to psychotic reactions if they take cannabis regularly.

Question 5

Murray (2005)

Answer 5

argues that cannabis consumption interacts with genetic susceptibility to schz

Question 6

Comer (2003) and Randrup & Monkuad (1996)

Answer 6

show evidence of studies conducted on animals that support the point that drugs can influence the DA levels of patients

Question 7

Degenhardt et al (2003)

Answer 7

• found that despite a rapid increase in cannabis use in Australia during 1980-2000 there is no evidence of an increase in psychosis in the Australian population during this time