2. The Desensitisation Hypothesis

Question 1

who’s theory was the desensitisation hypothesis? what does it base its theory on?

Answer 1

Dani and Heinemann’s - based on permenant changes to brain neurochemistry.

Question 2

what is the process outlines in the desensitisation hypothesis? (7) p.s. does not have to be perfect in wording, clear understanding needed.

Answer 2

• one subtype of acetylcholine receptor (AChR) is the nicotinic receptor (nAChR.)
• when it binds to nicotine, it becomes overstimulated and immediately shuts down.
• there are now fewer active receptors available, leading to desensitisation.
• the nucleus accumbens releases dopamine from the pleasure/reward system. creating the pleasurable effect of smoking.
• when smokers abstain from the drug for long periods of time, the drug is metabolised by the CYP2A6 gene.
• neurons become sensitised again, known as upregulation.
• this explains withdrawal and tolerance through permenant changes to brain chemistry.

Question 3

what is the supporting evidence for the desensitisation hypothesis?

Answer 3

Joseph McEvroy et al 1995 gave haloperidol to schizophrenics, a dopamine antagonist. All participants increased cigarette consumption, seeking dopamine from elsewhere.

Question 4

what are the counter arguments to the desensitisation hypothesis? (5 - minimum 3)

Answer 4

• Shiffman et al 1995 discovered that there are individual differences within nicotine addiction. Those that smoke less than 5 a day show no signs of withdrawal at abstinence.
• The research itself also offers a reductionist explanation as it shows no social explanation.
• Won Choi et al 2003 found that adolescents at school were most likely to become dependent if they perceived themselves to be underachieving at school.
• reductionist
• doesn’t acknowledge GABA or serotonin

Question 5

what can this be applied to?

Answer 5

NRT