(3) (a) Explanations for nicotine addiction: brain neurochemistry, including the role of dopamine

Published by admin on

AO1
Desensitisation hypothesis- Role of nAChRs; Desensitisation; Effect of dopamine

Nicotine regulation model- Resensitisation of neurons leads to upregulation, Upregulation leads to withdrawal syndrome, Chronic desensitisation increases tolerance.

Desensitisation hypothesis
1. Role of nAChRs- dopamine-producing neurons have acetylcholine receptors that also respond to nicotine.

2. Desensitisation- when nicotine binds to a nAChR… a) neuron is stimulated and produces dopamine b) receptors shut down within milliseconds and cannot respond to neurotransmitters (desensitisation) leading to fewer active neurons (downregulation).

3. Effect of dopamine- reward and pleasure (reduced anxiety, mild euphoria, increased alertness). Now associated w nicotine intake.

Role of nAChRs
Dopamine-producing neurons have acetylcholine receptors that also respond to nicotine.
Desensitisation
When nicotine binds to a nAChR…

a) Neuron is stimulated and produces dopamine

b) Receptors shut down within milliseconds and cannot respond to neurotransmitters (desensitisation) leading to fewer active neurons (downregulation).

Effect of dopamine
Reward and pleasure (reduced anxiety, mild euphoria, increased alertness).

Now associated w nicotine intake.

Nicotine regulation model
Resensitisation = upregulation- nicotine disappears from the body when smokers go without smoking for a prolonged period, nAChRs become functional again (resensitise) and more becomes available (upregulation).

Upregulation = withdrawal symptoms- more nAChRs become available but not stimulated = acute withdrawal (anxiety). Most sensitive, first cigarette therefore the most pleasurable, reactivates dopamine reward system.

Chronic desensitisation = tolerance- persistent desensitisation of nAChRs through repeated smoking = persistent decrease in the no. of active receptors, more nicotine for the same effects.

Resensitisation = upregulation
Nicotine disappears from the body when smokers go without smoking for a prolonged period, nAChRs become functional again (resensitise) and more becomes available (upregulation).
Upregulation = withdrawal symptoms
More nAChRs become available but not stimulated = acute withdrawal (anxiety). Most sensitive, first cigarette therefore the most pleasurable.

Reactivates dopamine reward system.

Chronic desensitisation = tolerance
Persistent desensitisation of nAChRs through repeated smoking = persistent decrease in the no. of active receptors.

More nicotine for the same effects.

Tolerance develops.

AO3
S: Research support (McEvoy et al. 1995); (Ray et al. 2008)

S: Practical value, NRT

L: Neurochemical explanations only consider dopamine.

L: Reductionist (Choi et al. 2003)

L: Individual differences (Shiffman 1995)

McEvoy et al. (1995)
Smoking behaviour in patients with SZ, some of whom were taking haloperidol, a dopamine antagonist drug treatment for SZ.

Treatment increases smoking in this sample of pps.

Self-medication, nicotine ‘hit’ by increasing dopamine release.

Ray et al. (2008)
Direct evidence for the importance of the dopamine reward system in brain-imaging studies.
(S) Research support
McEvoy et al. (1995)

Ray et al. (2008)

(S) Practical value, NRT
Greater understanding of neurochemistry = dev of treatments (NRT) in the form of patches and inhalers.

Practical benefits extend beyond nicotine addiction- co-morbid (depression, alcoholism).

Prospect of further research = advances in treatments for these co-morbid disorders.

Validity

(L) Neurochemical explanations only consider dopamine.
Considers only the role of dopamine, limited because there are many other neuro-mechanisms involved.

Complex interaction of several systems (GABA, serotonin pathways, and endogenous opioids).

Have to understand how it interacts with these other systems.

Reductionism v Holism

Choi et al. (2003)
Most adolescents who become dependent had peers who smoked or felt they were underachieving at school.
(L) Reductionist
Explain addiction at the most basic level (activity of neurotransmitter molecules), rather than at ‘higher’ levels (e.g. social and psychological influences).

Only around 50% of people who experiment with smoking become dependent.

Choi et al. (2003)

Crucial psych. factors overlooked in favour of brain neurochemistry?

Reductionism v Holism

Shiffman et al. (1995)
Studied ‘chippers’ – people who regularly smoked for long periods but do not become dependent.

Even those who smoked an avg. of 5/day did not show withdrawal symptoms.

(L) Individual differences
Shiffman et al. (1995)

Suggests- non-chemical factors protect some people from addiction. Such people smoke because of modelling and learning and their motivation has nothing to do with nicotine.

Questions emphasis placed on exclusively biological approaches.

Categories: Neurochemistry