explanations for nicotine addiction: brain neurochemistry Flashcards
what is acetylcholine (ACh) ?
a neurotransmitter that plays a key role in attention, arousal, muscle movement, etc.
what is nAChR?
nicotinic acetylcholine receptor - a subtype of ACh receptor that can be activated either by ACh or nicotine
where can lots of ACh receptors be found?
on the surfaces of many neurons in CNS
what happens when nAChRs are activated by nicotine molecules?
the neuron transmits dopamine, which is immediately followed by shutdown of nAChRs
what is downregulation?
a reduction in the number of active neurons
what leads to downregulation?
desensitisation of neuron
where are nAChRs concentrated?
ventral tegmental area (VTA)
where is dopamine transmitted when nAChRs are stimulated by nicotine?
dopamine is transmitted along mesolimbic pathway to nucleus accumbens (NA), triggering release of more dopamine from NA to frontal cortex
what are the mesolimbic + mesocortical pathways part of?
the brain’s dopamine reward system
what does the activation of the dopamine reward system result in?
pleasurable effects (e.g. mild euphoria, increased alertness, etc.)
what happens when a person doesn’t smoke for a prolonged period (e.g. at night) ?
nicotine disappears from the body
what happens when nAChRs become functional again?
dopamine neurons resensitise and become more available (upregulation)
what happens during resensitisation?
nAChRs become overstimulated by ACh (as there’s no nicotine to bind with them)
why is the first cigarette of the day often the most enjoyable?
sensitive nAChRs reactivate the dopamine reward system
how does the smoker avoid unpleasant withdrawal symptoms?
by smoking another cigarette
what creates a long-term desensitisation of nAChRs?
the constant cycle of daytime downregulation + nighttime upregulation
what does a continuous exposure of nAChRs to nicotine cause?
a decrease in number of active receptors, leading to tolerance development as a smoker needs more nicotine to get the same effects
what are 2 strengths of this explanation?
~ research support
~ real-world application
what are 2 limitations of this explanation?
~ it doesn’t fully explain withdrawal
~ biologically determinist
what did McEvoy et. al. study?
smoking behaviour in people with schizophrenia who were taking an antipsychotic drug (which blocks dopamine receptors in the brain, therefore reducing dopamine transmission)
what did McEvoy et. al. find?
people taking the drug showed a significant increase in smoking, presumably using it as a form of self-medication or to increase depleted dopamine levels
what is one counterpoint to ‘research support’?
reductionist explanation - explanations that only consider dopamine are limited
what did Watkins et. al. find as a counterpoint to McEvoy’s research?
nicotine addiction was also linked to GABA, serotonin, endogenous opioids etc. - therefore there is a complex interaction between several neurochemical systems
how does this explanation have a real-world application?
knowledge of neurochemistry can lead to new treatments (e.g. NRT), showing that the explanation has validity
