Nicotine Addiction & Brain Neurochemistry (AQA A Level Psychology): Revision Note

The desensitisation hypothesis & dopamine

• The desensitisation hypothesis of nicotine addiction suggests that prolonged exposure to nicotine leads to reduced sensitivity of nicotinic acetylcholine receptors

  • The desensitisation hypothesis is based on the action of nicotine in the brain and its effect on the neurotransmitter dopamine

• Nicotine molecules bind with nicotinic acetylcholine receptors (nAChRs), which normally bind with acetylcholine, and this causes the neuron to become stimulated and transmit dopamine

• nAChRs are concentrated in the ventral tegmental area (VTA) of the brain, and when they are stimulated by nicotine, dopamine is transmitted along the mesolimbic pathway to the nucleus accumbens

• Dopamine is also transmitted along the mesocortical pathway to be released in the frontal cortex

  • Together the mesolimbic and mesocortical pathways are part of the brain's reward and pleasure centre, and nicotine powerfully activates this system, resulting in pleasurable effects such as mood elevation, increased alertness and reduction of anxiety

• Immediately after nicotine binds (a matter of just milliseconds), the nicotinic receptor shuts down and temporarily cannot respond to neurotransmitters, so the neuron is said to be desensitised

  • This leads to downregulation, a reduction in the number of active neurons, because fewer receptors are available

• The more nicotine that is used, the more tolerance increases, which leads to even more nicotine being needed, and addiction is the result 

The nicotine regulation model

• If nicotine is not used for some time, then it is metabolised by the body and excreted by the kidneys

  • More nicotinic receptors become functional again, so dopamine neurons resensitise and more become available, a process known as upregulation

• More receptors are available and overstimulated by acetylcholine, which contributes to an acute withdrawal syndrome with symptoms including anxiety and agitation

  • At this point, after a period of abstinence, the receptors are at their most sensitive, which is why smokers often describe the first cigarette of the day as the most enjoyable; it re-activates the dopamine reward system

• The withdrawal symptoms are worse if nicotine use has been prolonged, as long-term use of nicotine increases the number of nicotinic acetylcholine receptors, increasing the sensitisation and the subsequent agitation and anxiety

Research which investigates nicotine addiction and brain neurochemistry

• McEvoy et al. (1995) studied smoking behaviour in people with schizophrenia being treated with haloperidol, a dopamine antagonist which blocks dopamine receptors in the brain, and found that treatment increased smoking in this sample

  • This suggests participants were attempting to achieve the nicotine 'hit' by increasing dopamine release, supporting the role of dopamine in nicotine addiction

• Domino (2004) used fMRI scans to track the blood flow in the nucleus accumbens, amygdala, and hippocampus immediately after smoking the first cigarette in the morning and found that the first cigarette had the largest effect, supporting the desensitisation hypothesis

• Cosgrove et al. (2014) used PET scans to compare the brains of men and women while smoking and found that the dopamine effect took place in different regions of the brain, suggesting that men and women might smoke for different reasons 

Evaluation of nicotine addiction and brain neurochemistry

Strengths

• The role of dopamine could explain how there appears to be a genetic link to addiction

  • The release of dopamine may lead some individuals to feel more reward from using nicotine than others, and this difference in the dopaminergic pathway may be inherited

• A greater understanding of neurochemistry can lead to the development of new treatments for nicotine addiction, such as nicotine replacement therapy in the form of patches and inhalers, with research even raising the possibility of nicotine immunisation

  • Some diseases have high co-morbidity with nicotine use, such as schizophrenia, depression and alcoholism, all of which are strongly associated with continued smoking, so research which offers more effective treatments for nicotine addiction also holds the prospect of advances in treating these co-morbid disorders

Limitations

• The research evidence in this area often comes from animal experiments, meaning the findings may not be generalisable to humans

• Any explanation considering only the role of dopamine is limited, as research increasingly shows that there are many other neurochemical mechanisms involved, including GABA and serotonin, plus other systems such as endogenous opioids (endorphins, the brain's natural painkillers)

  • However, Berrendero et al. (2010) point out that the dopamine system is nevertheless central to the neurochemistry of nicotine addiction and these other systems all interact with it to have their effects

Issues & Debates

• Focusing only on neurochemical mechanisms is biologically reductionist, as it ignores psychological and social factors (e.g., stress, peer pressure, habits) that influence smoking

  • A more holistic understanding of addiction would consider how brain chemistry interacts with environment and individual experience

• Cosgrove et al. (2014) found gender differences in the neural response to nicotine, suggesting that previous theories may have overlooked sex-based biological differences

  • This leads to a gender bias in addiction models and treatments