Addiction - Explanations for Nicotine Addiction Flashcards
What are the key features of the desensitisation hypothesis?
- the role of nAChRs
- desensitisation caused by nicotine
- effect of dopamine
What is the role of nAChRs?
Dani and Heinemann’s (1996) hypothesis focuses on the neurotransmitter dopamine.
Some neurons that produce dopamine are in the ventral tegmental area (VTA) of the brain.
These neurons have acetylcholine (ACh) receptors that also respond to nicotine - these receptors are called nicotinic receptors (nAChRs).
How is desensitisation caused by nicotine?
When nicotine binds to a nAChR:
- The neuron is stimulated and produces dopamine.
- The receptors shut down within milliseconds and cannot respond to neurotransmitters = desensitisation of the neuron (no longer responds) leading to downregulation (fewer active neurons available).
What is the effect of dopamine?
When the neurotransmitter dopamine is released from the VTA it is transmitted along the:
- Mesolimbic pathway to the nucleus accumbens to be released in the frontal cortex.
- Mesocortical pathway to be released in the frontal cortex.
The dopamine system creates a sense of reward and pleasure (e.g. reduced anxiety, mild euphoria, increased alertness).
This is now associated with intake of nicotine.
What are the key features of the nicotine regulation model?
- resensitisation of neurons leads to upregulation
- upregulation leads to withdrawal symptoms
- chronic desensitisation increases tolerance
What does the resensitisation of neurons lead to?
When smokers go without nicotine for a prolonged period (e.g. when asleep), nicotine disappears from the body.
nAChRs become functional again, so neurons resensitise and more become available (upregulation).
What does upregulation lead to?
Because more nAChRs are available but not stimulated, the smoker experiences acute withdrawal syndrome (e.g. anxiety).
Meanwhile nAChRs are at their most sensitive, which is why smokers describe the first cigarette of the day as the most pleasurable - it reactivates the dopamine reward system.
This explains how dependence to nicotine is maintained - the smoker is motivated to avoid unpleasant withdrawal symptoms.
What does chronic desensitisation do?
Persistent desensitisation of nAChRs through repeated smoking leads to a permanent decrease in the number of active receptors - requiring more nicotine for the same effects. Therefore, tolerance develops.
What are the strengths of brain neurochemistry as an explanation for nicotine addiction?
- there is supporting research evidence
- real-life applications
What are the weaknesses of brain neurochemistry as an explanation for nicotine addiction?
- only consider dopamine
- reductionist
- individual differences
What supporting research evidence is there for brain neurochemistry?
McEvoy et al. (1995) studied smoking behaviour in patients with schizophrenia, some of whom were taking haloperidol, a dopamine antagonist drug treatment for schizophrenia.
Haloperidol treatment increased smoking in this sample of participants. It appears that this was a form of self-medication, an attempt to achieve the nicotine ‘hit’ by increasing dopamine release.
There is also more direct evidence for the importance of the dopamine reward system in brain imaging studies (Ray et al. 2008).
What real-life applications have been developed due to brain neurochemistry?
A greater understanding of neurochemistry has led to the development of treatments such as nicotine replacement therapy (NRT) in the form of patches and inhalers.
But the practical benefits of understanding go beyond nicotine addiction. Some diseases have high co-morbidity rates with nicotine use (e.g. depression, alcoholism).
This raises the prospect of further research leading to greater advances in treatments for these co-morbid disorders.
How do the neurochemical explanations only consider dopamine?
An explanation of nicotine addiction that considers only the role of dopamine is limited because there are many other neuro-mechanisms involved.
The current picture shows a vastly complex interaction of several systems such as GABA and serotonin pathways, and endogenous opioids.
So although dopamine is central to nicotine addiction neurochemistry, we have to understand how it interacts with these other systems.
How are the neurochemical explanations reductionist?
Neurochemical explanations explain addiction at the most basic level of the 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) found that most adolescents who become dependent had peers who smoked or felt they were underachieving at school.
It could therefore be argued that crucial psychological factors are in danger of being ignored by focusing on brain neurochemistry.
What individual differences are there with brain neurochemistry?
Shiffman et al. (1995) studied ‘chippers’, people who regularly smoke for long periods but who do not become dependent. Even those who smoked an average of five per day did not show withdrawal symptoms.
It is suggested that non-chemical factors protect some people from addiction. Such people smoke because of modelling and learning and their motivation has nothin to do with nicotine.
This questions the emphasis places on exclusively biological approaches to understanding addiction to smoking.