Describe and evaluate one or more of the following explanations for nicotine addiction: brain neurochemistry, learning theory.

AO1: Who came up with the desensitisation hypothesis?

Dani and Heinemann (1996)
They focused on neurons that produce the neurotransmitter ACh - causes physiological arousal and reward mechanisms

AO1: Nicotine

Nicotine is the main active ingredient in tobacco → nicotine can have a range of different effects

• Tranquilisation

• Decreased irritability

• Increased alertness

• Improved cognitive function

These become less evident among regular smokers as they’ve built up a tolerance.

Nicotine has both stimulant and relaxation effects → Nicotine paradox - this means it can invigorate at times and calm at others

HOWEVER, the paradox explaination that smoking only appears relaxing is because smokers are in a constant state of mild nicotine withdrawl.

AO1: What does nicotine do?

1-2mg of nicotine per cigarette → This is absorbed into the lining of the mouth, nose and by inhalation into the lungs → reaches its peak levels in the bloodstream in less than 10 seconds

→ Reward pathways activate a pleasure feeling

• It then attatches to the neurons in the region of the brain called the ventral tegmental area (VTA)

• Nuclens accumbens (NAc): triggers release of the neurotransmitter dopamine.

• The release of glucamate is also stimulated → this triggers an additional release of dopamine which releases feelings of pleasure - the desire to repeat the behaviour leads to addiction

AO1: Why does dopamine remain high after nicotine stimulus ends?

Glucamate and GABA play a role

• Glucamate speeds up activity in the neurons

• GABA slows down activity in the neurons

Nicotine causes the glucamate to speed up dopamine release BUT prevents GABA from slowing it down

This happens while cigarettes also contain an unknown substance that blocks action in the MAOs (breaks down dopamine after its effect) because it doesnt occur = dopamine levels rising → stengthens smoking habits

AO3: Real world application (Support)

Allowed for the development of new treatments

Explanation has increased our understanding of neurochemistry behind nicotine addiction. This led to the development of effective nicotine addiction treatments eg nicotine replacement therapy.

Works by delivering a controlled dose of nicotine ,which binds to the nAChRs, this stimulates the release of dopamine and mimics effects of nicotine in cigarettes - This satisfies cravings and allows users to control and reduce withdrawal symptoms by gradually reducing dose of nicotine, making quitting easier.

Explanation has led to effective nicotine addiction treatments → high practical value.

AO3: Research support

Research found that smoking behaviour increased in participants taking an antipsychotic drug (which blocks dopamine receptors in the brain, reducing dopamine transmission)

It suggests that people smoke cigarettes aiming to increase their dopamine levels via nicotine

This supports claims of tge neurochemical explanation that dopamine plays a key role in nicotine addiction - valid explanation.

AO3: Biologically deterministic

This suggests that nicotine addiction is inevitable once someone starts smoking due to automatic chemical processes which occur in the brain when smoking, that we have no control over.

However many people smoke without becoming addicted, and find quitting very easy without. experiencing withdrawal symptoms.

Suggests there is an elements of free will in nicotine addiction.

Brain neurochemistry explanation takes an unrealistically deterministic view.

AO3: Biologically reductionist (Limitation)

Explanation reduces nicotine addiction to the level of neurotransmitters and receptors

HOWEVER, alternative explanations eg learning theory have shown that addictions are learnt and maintained via classical and operant conditioning

The neurochemical explanation completely ignores the influence of non biological factors like social factors and learning on nicotine addiction

This implies that nicotine addiction is much more complex than the neurochemical explanation suggests, therefore the explanation is over-simplistic & limits our understanding.

AO1: What is the main idea of the learning theory as an explanation for nicotine addiction?

Suggests that nicotine addiction is a learned behaviour which can be explained in terms of operant conditioning and/or classical conditioning

AO1: Explain operant conditioning as positive reinforcement for the learning theory explanation for nicotine addiction

When smoking, nicotine stimulates the release of dopamine along the mesolimbic pathway into the nucleus accumbens which stimulates the release of dopamine from the NA into the frontal cortex

• Creates pleasurable feelings of euphoria

These effects are rewarding which positively reinforces their smoking behaviour making it likely to be repeated

Positive reinforcement explains why people start smoking

AO1: Explain operant conditioning as negative reinforcement for the learning theory explanation for nicotine addiction

Negative reinforcement expains how a smokers addiction to nicotine is maintained

When a smoker stops consumption of nicotine this leads to withdrawl symptoms which has unpleasant effects (eg. disturbed sleep, depression) by smoking more the smoker avoids these symptoms

This negatively reinforces the smokers behaviour making them more likely to smoke again.

AO1: Explain primary reinforcer for the learning theory explanation for nicotine addiction

• Smoking is a primary reinforcer because it is intrinstically rewarding

Intrinsically rewarding: the rewarding feeling of smoking is not learned but rather is biologically determined due to the effects of nicotine on the brain’s dopamine reward system

AO1: Explain secondary reinforcer for the learning theory explanation for nicotine addiction

Other stimuli present when smoking (eg lighters, location, people you smoke with) become associated with nicotine via classical conditioning.

So they produce a conditioned response of pleasurable effects (the same effect produced by nicotine when smoking), even when not smoking.

These cues are known as secondary reinforcers.

The rewarding feeling produced by secondary reinforcers is learnt.

AO3: Real world application – development of treatments (Support)

Allowed us to understand the role which classical conditioning plays in nicotine addiction.

Led to development of treatments which are based on classical conditioning principles.

E.g., aversion therapy uses counterconditioning to treat nicotine addiction by associating smoking with an unpleasant stimulus e.g., an electric shock

High practical value as it has led to effective nicotine addiction treatments.

AO3: Research support - role of operant conditioning

Rats had the option to lick 2 different water spouts – one provided some nicotine and the other didn’t.

Found that rats licked nicotine related water spout significantly more and that the frequency of licking the nicotine spout increased over time.

Suggests that pleasurable effects of nicotine positively reinforce the individuals behaviour of consuming nicotine as suggested by learning theory.

Increases validity of learning theory.

AO3: Animal studies (Limitation)

Most research was done on non human animals (Rats)

Cognitive systems which influence learning are much more complex in humans than in animals so the process of learning nicotine addiction in humans is likely to be much more complex than in animals.

So animal studies are unrepresentative of human nicotine addiction and can’t be generalised to humans confidently.

Animal studies are also unethical - do not protect the animal from harm but instead put them under harm (risk of developing nicotine addiction & its negative effects).

Learning theory is supported by unethical and unrepresentative research of human addiction so we can’t be sure that learning theory is a valid theory of human nicotine addiction.

AO3: Environmentally reductionist (Limitation)

Reduces nicotine addiction solely down to learning experiences.

However research has shown that some people have a genetic vulnerability to developing an addiction e.g. those with low levels of D2 receptors or those with high functioning CYP2A6 enzymes.

Ignores influence of genetics of nicotine addiction = over simplistic explanation.

Diathesis stress model which considers interaction between genetic vulnerability and environmental triggers would provide a more comprehensive explanation.