Addiction - Explanations for Nicotine Addiction Flashcards

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1
Q

What are the key features of the desensitisation hypothesis?

A
  • the role of nAChRs
  • desensitisation caused by nicotine
  • effect of dopamine
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2
Q

What is the role of nAChRs?

A

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).

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3
Q

How is desensitisation caused by nicotine?

A

When nicotine binds to a nAChR:

  1. The neuron is stimulated and produces dopamine.
  2. 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).
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4
Q

What is the effect of dopamine?

A

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.

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5
Q

What are the key features of the nicotine regulation model?

A
  • resensitisation of neurons leads to upregulation
  • upregulation leads to withdrawal symptoms
  • chronic desensitisation increases tolerance
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6
Q

What does the resensitisation of neurons lead to?

A

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).

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7
Q

What does upregulation lead to?

A

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.

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8
Q

What does chronic desensitisation do?

A

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.

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9
Q

What are the strengths of brain neurochemistry as an explanation for nicotine addiction?

A
  • there is supporting research evidence

- real-life applications

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10
Q

What are the weaknesses of brain neurochemistry as an explanation for nicotine addiction?

A
  • only consider dopamine
  • reductionist
  • individual differences
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11
Q

What supporting research evidence is there for brain neurochemistry?

A

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).

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12
Q

What real-life applications have been developed due to brain neurochemistry?

A

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.

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13
Q

How do the neurochemical explanations only consider dopamine?

A

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.

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14
Q

How are the neurochemical explanations reductionist?

A

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.

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15
Q

What individual differences are there with brain neurochemistry?

A

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.

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16
Q

What are the key features of operant conditioning as an explanation for nicotine addiction?

A
  • positive reinforcement - mild euphoria
  • mild euphoria caused by the dopamine system
  • negative reinforcement - avoid withdrawal symptoms
17
Q

How does positive reinforcement explain nicotine addiction?

A

If the consequence of a behaviour is rewarding to an individual, then that behaviour is more likely to occur again.

Smoking can create feelings of mild euphoria which positively reinforce the smoking behaviour.

18
Q

How is mild euphoria caused by the dopamine system?

A

Nicotine is a powerful reinforcer because of its physiological effects on the dopamine reward system in the mesolimbic pathway.

Nicotine stimulates the release of dopamine which produces the feeling of mild euphoria.

19
Q

How does negative reinforcement explain nicotine addiction?

A

Cessation of nicotine use can lead to an acute withdrawal syndrome including such symptoms as disturbed sleep, agitation, poor concentration and mood disturbances.

Therefore addiction is maintained because smoking another cigarette is negatively reinforcing - it stops the unpleasant stimulus (withdrawal symptoms).

20
Q

What are the key features of classical conditioning as an explanation for nicotine addiction?

A
  • smoking is a primary reinforcer as it is intrinsically rewarding
  • secondary reinforcers include pubs, friends, lighters, smells, etc.
  • cue reactivity: cravings are triggered by cues related to smoking
21
Q

How is smoking a primary reinforcer?

A

Smoking is intrinsically rewarding (not learned). It doesn’t have to be learned because of the biologically-determined effects of nicotine on the dopamine reward system.

The pleasure created by nicotine reinforces the behaviour so the individual is more likely to smoke again.

22
Q

What secondary reinforcers are involved in nicotine addiction?

A

Any other stimuli present at the same time as (or just before) smoking (and intake of nicotine) become associated with the pleasurable effect of smoking (i.e. classical conditioning has taken place). These stimuli become secondary reinforcers (rewarding in their own right).

Certain environments (e.g. pubs) and certain people or objects (e.g. a lighter) create a sense of anticipation and pleasure and thus become secondary reinforcers.

Even the seemingly harsh feeling of smoke hitting the back of the throat can become a secondary reinforcer because it is associated with the pleasurable impact of nicotine.

23
Q

What is cue-reactivity?

A

The secondary reinforcers also act as cues, because their presence produces a similar response to nicotine itself. This is called cue reactivity and is indicated by three main elements:

  1. Self-reported desire to smoke.
  2. Physiological signs of reactivity to a cue (e.g. heart rate).
  3. Objective behavioural indicators when a cue is present (e.g. how many ‘draws’ are taken on the cigarette).
24
Q

What are the strengths of the learning theory as an explanation for nicotine addiction?

A
  • support from non-human animal studies
  • research support for cue reactivity
  • real-life application of the theory
  • gender differences can also be explained
25
Q

What are the weaknesses of the learning theory as an explanation for nicotine addiction?

A
  • cannot explain why some people do not become addicted
26
Q

What support is there for the learning theory as an explanation for nicotine addiction?

A

Levin et al. (2010) gave rats the choice of self-administering doses of nicotine or water by licking one of two water spouts (one with nicotine).

The rats licked the nicotine water spout significantly more often. This behaviour increased in frequency with every subsequent training session.

The effects of nicotine positively reinforce nicotine self-administration in rats, suggesting a similar mechanism in humans.

27
Q

What research support is there for reactivity?

A

Carter and Tiffany’s meta-analysis included measures of self-reported craving and physiological arousal in dependent and non-dependent smokers, following exposure to smoking-related cues.

The researchers found that dependent smokers reacted strongly to cues (e.g. lighters), reporting high levels of craving and demonstrating higher levels of physiological arousal.

The findings were consistent with the predictions of cue reactivity theory and therefore support the theory.

28
Q

What real-life applications are there of the learning theory as an explanation for nicotine addiction?

A

Aversion therapy works on the basis of counterconditioning nicotine addiction by associating the pleasurable effects of smoking with an aversive stimulus such as a painful electric shock.

Smith (1988) found that 52% of participants who gave themselves electric shocks whenever they engaged in smoking-related behaviours were still abstaining.

Such effective applications of learning theory have measurable and significant practical benefits in terms of reducing NHS spending and improving health.

29
Q

How can gender differences also be explained by the learning theory as an explanation for nicotine addiction?

A

Carpenter et al. (2014) suggest females struggle to give up smoking because they are more sensitive to smoking-related cues, making relapse more likely.

The concept of self-efficacy would suggest that female smokers have less confidence in their ability to give up smoking and this undermines their attempts.

Self-efficacy is learned which means that gender differences can be explained in terms of learning, thus supporting this approach.

30
Q

Why can’t the learning approach explain why some people do not become addicted?

A

Even though positive reinforcement is a strong explanation, not everyone who experiments with smoking becomes dependent.

Many adolescents smoke cigarettes occasionally, but few are dependent to the extent that they experience withdrawal symptoms.

This is a challenge for any theory seeking to explain addiction; there are likely to be several causes of smoking behaviour.