Neurochemical explanation for nicotine addiction

• The desensitisation hypothesis

  Proposed initially by Dani & Heinemann (1996), the desensitisation hypothesis focuses on how exposure to nicotine contributes to the downregulation of the brain’s reward system.

  This process involves both the neurotransmitters Acetylcholine (ACh) and Dopamine.
• Acetylcholine 

  Acetylcholine is an excitatory neurotransmitter thought to be linked to arousal and reward

  ACh also plays a role in all nervous system function and therefore ACh receptors are present on many neurons throughout the nervous system. 

  Transmission of ACh works as it does with every other neurotransmitter and stimulates action potentials in the postsynaptic neuron if sufficient
• Acetylcholine & nicotine

  One subtype of ACh receptor is called to nicotinic acetylcholine receptor (nAChR). These receptors are able to respond to acetylcholine AND nicotine.
• Acetylcholine & nicotine

  When nAChRs are activated by nicotine molecules, the neuron is stimulated and transmits dopamine. 

  However

  The neuron then immediately enters a state of shutdown wherein it is temporarily not able to respond to any neurotransmitters. 

  At this point the neuron is said to be desensitised. This leads to downregulation - a reduction in the availability and number of active neurons
• Desensitisation hypothesis - Dopamine

  nAChRs are concentrated in the ventral tegmental area (VTA) of the brain. When stimulated by nicotine, the dopamine released down two pathways:

  Mesolimbic pathway

  Mesocortical pathway
• 1. Dopamine is transmitted along the mesolimbic pathway to the nucleus accumbens (NA). The NA then releases more dopamine directly into the frontal cortex
  2. 2. At the same time, dopamine is also transmitted along the mesocortical pathway into the frontal cortex
• Desensitisation hypothesis - Dopamine

  This process is particularly important in the Nucleus Accumbens. This is the reward centre. 

  Nicotine addiction occurs because the nAChR process triggers dopamine in the NA.

  Nicotine is a very powerful stimulant of the dopamine system creating the rewarding/pleasurable effects that accompany its use.  

  Constant exposure of dopamine = desensitisation and tolerance levels being built (need more to feel the same effect)
• What happens to nicotine in the body after a long period without smoking?

  Nicotine is fully metabolised and disappears
• What occurs to nACh receptors when nicotine is absent for a long time?

  They undergo upregulation and become functional
• What happens to dopamine neurons during nicotine withdrawal?

  They become resensitised
• Why does withdrawal occur when nicotine is absent?

  Lack of nicotine overstimulates sensitive nAChRs
• How does increased ACh affect dopamine levels during withdrawal?

  Increased ACh leads to decreased dopamine
• How do smokers describe the first cigarette of the day?

  As the best cigarette
• Why do smokers find the first cigarette of the day particularly satisfying?

  It strongly reactivates the dopamine system
• Nicotine regulation model - dependence & tolerance 

  Constant repetition of this day-time downregulation and nighttime upregulation over time creates chronic desensitisation of nicotinic receptors which can only be overcome by increasing nicotine (tolerance) 

  Long term exposure to nicotine can cause permanent changes to the brain’s neurochemistry, decreasing the total number of active receptors.
• AO3

  + Human research support

  Joseph McEvoy et al (1995) studied smoking behaviour in people with schizophrenia who had been prescribed the antipsychotic drug Haloperidol. This drug is a dopamine antagonist - blocking the neurotransmitter. The people taking the drug showed a significant increase in smoking (presumably as a form of self-medication to increase their depleted levels of dopamine)

  This supports the role of dopamine in nicotine addiction.
• AO3

  + Real world support

  This understanding of neurochemistry has lead to new treatments. Nicotine replacement therapy (NRT) was developed after the establishment that nicotine was the addictive component in cigarettes. As such patches, gum, vapes etc. all deliver controlled doses of synthetic nicotine to manage addiction by acting on nAChRs in the same way the nicotine in cigarettes does. 

  This effectively reduces withdrawal symptoms and allows people to quit smoking.
• What does the neurochemical explanation suggest about withdrawal symptoms?

  Withdrawal is due to lack of nicotine
• Who suggested that environmental factors and personality are greater determinants of withdrawal symptoms?

  David Gilbert
• What personality dimension is linked to worse withdrawal symptoms?

  Neuroticism
• In what year did David Gilbert make his suggestion about withdrawal symptoms?

  1995
• What are the key factors influencing withdrawal symptoms according to Gilbert?

  • Lack of nicotine (neurochemical explanation)
  • Environmental factors
  • Individual's personality
• How do individuals with high neuroticism experience withdrawal symptoms compared to those who are emotionally stable?

  They generally experience worse withdrawal symptoms
• What does the neurochemical explanation fail to fully explain?

  Withdrawal symptoms
• Model paragraph

  One limitation of the neurochemical explanation of addiction is that it is biologically deterministic. This theory suggests that we become addicted to nicotine because of neurochemical changes to dopamine that are out of our control. This would mean that nicotine addiction is inevitable in all people who start smoking. However, not all people who start smoking become dependent and some may find it easier to quit than others (Gilbert, 1995). Therefore this level of determinism is not an entirely appropriate explanation for nicotine addiction