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Nicotine

Uni of Notts, Addiction & The Brain, first year

TermDefinition
Legal differences in marketing of cigarettes Originally advertised to help WW2 soldiers cope with stress but now they must be bought in packs of >19 with the voted most ugly colours, health warnings, minimal branding, & graphic medical pictures of smoking damage
Economic damage of tobacco products UK government spends up to £19bn per annum on treating tobacco related illnesses & helping overcome addiction (studies show it's potentially more addictive than heroin)
Cultivation & properties of tobacco plants Grown only in mild, sunny climates. Roots synthesise neurotoxic insecticide which are transported to leaves, this makes up 0.6-3% of their dry weight
Pharmacology of smoking cigarettes 6-11mg nicotine per cigarette but only 1-3mg is absorbed. It binds to acidic tar molecules to rapidly & efficiently diffuse across the alveolar membrane to the bloodstream where it crosses the BBB in high concentration
How the pharmacology of non-smoked tobacco products differ from cigarettes Since burning tobacco leaves produces the tar, non-smoked products require significantly higher nicotine concentrations to have similar effects but can't replicate the same spike of nicotine release & instant high of cigarettes
Neural mechanism of nicotine activates nACh receptors in the pedunculopontine nucleus (PPT) to cause an action potential, stimulating dopaminergic VTA cells to increase dopamine concentration in the nucleus accumbens
Nicotinic VTA excitation study in mice Fa et al. (2000) Administered tobacco smoke to mice & measured VTA excitability using microelectrodes but when antagonist mecamylamine is administered, excitability decreases
Connection of mesolimbic pathway to survival behaviour Routtenberg & Lindy (1965) Rats with intracranial electrodes to stimulate the mesolimbic pathway when they press a lever will forgo natural rewards such as food & sex for stimulation even to the point of starvation
Connection between nicotine & dopamine release study in rats David (2006) Intracranial injections of nicotine to VTA using a Skinner box increased dopamine concentration in the nucleus accumbens but they stopped this behaviour when dopamine or ACh antagonists are administered
Effects of age on dependence Levin et al. (2003) Adolescents up to 25 years old who tried tobacco products are more likely to become addicted. Adolescent rats self-administering worked harder for nicotine & took higher doses
DSM dependence criteria Tolerance: Higher dose for same effect Withdrawal: Taking in the morning to help wake up Dose escalation: Using more tobacco than intended (chain smoking) Difficulty cutting down: Despite financial or medical issues
Prevalence of nicotine dependence 60% of users meet DSM criteria. Many people try it at least once & nearly 1/3 of users become dependent at some point but this also depends on vulnerabilities
Genetic impact on addiction susceptibility Variation in nicotine-specific hydrolytic enzymes & receptors affect rate of metabolism. Slower metabolism means individuals smoke less cigarettes for the same effect decreasing likelihood of addiction
Withdrawal symptoms (4) Urges & cravings, anxiousness & irritability, restlessness & difficulty staying focused, insomnia
Challenges of achieving long-term abstinence Smokers adjust dosage to maintain nicotine levels & prevent withdrawal. When trying to quit, relapses are likely to occur when the drug is accessible & allowed to be taken (situational variables)
Nicotine replacement therapy (+a disadvantage) Using alternative sources of nicotine, maintaining nACh receptor occupancy to reduce cravings. Alternatives include patch + gum, spray, lozenges, inhalators. This may lead to transfer dependence
Antidepressant therapy (+a disadvantage) Using selective dopamine & noradrenalin reuptake inhibitor bupropion/Zyban to counteract emotional withdrawal. The 12 month abstinence success rate is low with 2% of placebo trials successful
Habit based accounts Automatic drug-seeking behaviour driven by situational variables with insensitivity to the outcome
Stimulus response theory Pavlovian conditioning theory. Nicotine as the UCS with the sight, smell, & action of lighting the cigarette as the CS to reinforce drug-seeking behaviour
Insensitive salience (attentional bias) theory (+Stroop test results) Stimuli relating to the drug become high priority for attention & wanting it despite pleasure fading. Addicts were slower to name colours of words relating to drugs on the Stroop test. Greater attention bias correlates with worse clinical outcomes
Outcome devaluation studies Testing if behaviour is habit or goal directed by first supporting a neutral behaviour with a reward then changing the environment to 1 where the reward is freely accessible but the stimulus is still there. If they continue the behaviour, it's habit based
Goal directed accounts Deliberate behaviours based on expectancy theory of the value of outcomes
Example of stimulus devaluation (lithium chloride) LiCl causes sickness in rats, adding it to sucrose will devalue the reward & stop them taking it showing goal direction however, devaluing drugs doesn't work showing habit direction
Refutation of habit based accounts of nicotine addiction: Cravings Despite cravings being compulsive, the decision to seek out a drug despite consequences or lack of pleasure is a conscious decision. No model can account for all available nicotine data
Phenomenon accompanying cravings A mental image of taking the drug & feeling its positive effects showing a schema of drug expectations leading to drug seeking behaviour
Expectancy theory Behaviour is goal directed but driven by learned outcomes. Classical conditioning only causes a response with accompanying mental image. Knowledge of benefits of a behaviour make it more likely to be acted out
Created by: Beech47
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