Nicotine Addiction - Brain Neurochemistry Flashcards

1
Q

Desensitisation hypothesis

A
  • Dani and Heinemann (1996)

- focuses on brain neurochemistry, specifically dopamine-producing neurons

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2
Q

Dopamine-producing neurons

A
  • have receptors on their surfaces which bind to another neurotransmitter, acetylcholine (ACh)
  • when this binding happens, communication across synapses can take place
  • when enough ACh molecules bind with receptors, an electrical impulse can continue from the presynaptic to the post synaptic neuron
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3
Q

nAChR

A
  • subtype of ACh
  • found in the ventral tegmental area of the brain
  • both nicotine and ACh can bind with it
  • if nicotine binds, the neuron becomes stimulated and transmits dopamine along the mesolimbic pathway to the nucleus accumbens
  • the NA and neocortical pathway are part of brain’s reward system, meaning that when activated by nictotine, it results in pleasurable effects e.g. mild euphoria, reduced anxiety, alertness
  • however, once this happens, the nicotinic receptor shuts down and cannot respond to neurotransmitters for a short while
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4
Q

desensitisation

A
  • when the receptor shuts down after having bound to nicotine and sending nicotine, it is said to have desensitised
  • this leads to downregulation, which is a reduction in the number of active neurons due to fewer being available
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5
Q

nicotine regulation model

A
  • when a person is still smoking, nicotinic receptors are desensitised, meaning that craving and withdrawal symptoms don’t present themselves
  • however, if a smaller goes for a prolonged period of time without nicotine, such as when they go to sleep, nicotine dissipates from the body
  • most of the nicotinic receptors become functional again, i.e. dopamine neurons resensitise and become available, which is known as upregulation
  • more nAChRs are available but not being stimulated, which means that the smoker will experience acute withdrawal symptoms e.g. anxiety, agitation
  • this is therefore why a smoker will call their first cigarette of the day their most enjoyable, since it reactivates the dopamine reward system
  • this is why a nicotine dependence is maintained
  • the smoker wants to avoid unpleasurable physiological and psychological withdrawal symptoms, and the way that they can do this is by having another cigarette
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6
Q

Chronic desensitisation of nAChR

A
  • caused by repetition of the cycle of daytime down regulation and nighttime up regulation
  • permanent changes to the brain’s neurochemistry is caused by continuous exposure of nAChRs to nicotine
  • tolerance develops since the smoker has to smoke more to get the same effects
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7
Q

(+) EVAL - research evidence

A
  • there is indirect support for the role of neurochemistry in nicotine addiction from research with humans
  • McEvoy et al. (1995) examined smoking behaviours of patients with schizophrenia and he found that haloperidol, a dopamine antagonist which blocks dopamine receptors in the brain, treatment increased smoking within the participants
  • this was a form of self-medication, an attempt to achieve the nicotine hit by increasing dopamine release
  • Ray et al. (2008) found support for the importance of the dopamine reward system in the mesolimbic pathways through brain-imaging studies
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8
Q

(+) EVAL - real-life application

A
  • thanks to a greater understanding of neurochemistry, new treatments can be developed for nicotine addiction, such as nicotine replacement therapy (NRT)
  • this comes in the form of patches and inhalers
  • the possibility of nicotine immunisation also comes from research
  • potential practical benefits of a greater understanding of neurochemistry may go even further than nicotine addiction, since some diseases have a high-comorbidity with nicotine use
  • e.g. depression, schizophrenia and alcoholism
  • these disorders are all strongly associated with continued smoking
  • research offering more effective treatments for nicotine addiction therefore also holds out the prospect of greater advances in treatment for co-morbid disorders
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9
Q

(-) EVAL - limited explanation

A
  • one issue with this approach is that all the explanations only consider the role of dopamine, which means that they are limited because research increasingly shows that there are many other neurochemical mechanisms involved in addiction
  • instead, vastly complex interactions between several neurochemical systems, incl. neurotransmitter pathways and other systems such as endogenous opioids make up the current picture for addiction
  • Berrendero et al. (2010) on the other hand points 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
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