Drugs of abuse. CNS stimulants. Drugs of abuse: CNS Stimulants. Cocaine. Absorption of cocaine (pharmacokinetics) 28/10/2014.
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1 Learning outcomes Drugs of abuse Drugs of abuse: CNS Stimulants Dr B.Vahabi Identify different CNS stimulant drugs Explain the mechanism of action by which CNS stimulant drugs mediate their effects and why they create dependence and tolerance CNS stimulants: Cocaine, Caffeine Opiates: Heroin Opium Drugs of abuse Recreational drugs: Nicotine, Cannabis MDMA (Ecstasy) CNS Depressants: Alcohol Benzodiazepines CNS stimulants Can increase alertness and intensify moods Drug withdrawal negative moods/lethargy Have a high addiction potential Tolerance is developed readily Regular users often develop psychobiological problems Limited clinical use Cocaine Cocaine is found in leaves of coca plant (Erythroxylon coca) In 1990, 11% of US population reported using the drug at least once During 2000s its use has become more widespread, particular among the young Also known as: coke, crack, base, free base, rock, toot coca, snow etc. Can be sniffed/snorted, injected (hydrochloride salt) or smoked (crack) Absorption of cocaine (pharmacokinetics) Readily absorbed by many routes Hydrochloride salt can be used orally, intra-nasally or by intravenous injection Intravenous injection rapid effect Free-base form (crack) produces an effect similar to intravenous use Cocaine is metabolised by plasma esterases short half life Metabolites are deposited in hair 1
2 Mechanism of action of cocaine Inhibits catecholamine reuptake by the noradrenaline and dopamine transporters Results in increased presence of neurotransmitter in synapse greater postsynaptic stimulation Main neurotransmitters affected dopamine and noradrenaline Effect of cocaine on the mesolimbic reward pathway Acute effects of cocaine Intense euphoria Sympathomimetic effects lead to: Increased heart rate Faster breathing Increased body temperature Redistribution of blood from gut to muscle Alertness and wakefulness Increased confidence and strength Heightened sexual feelings Negative feelings can also be enhanced Irritability, suspiciousness, power and or invincibility extreme dangerous behaviour Associated with acts of violence Motor tics/ repetitive movements Overdose can result in convulsions/ hypertension/ hyperthermia and cardiac rhythm disturbances respiratory depression death Chronic effects of cocaine 1 CNS effects Neuroadaptive changes (in the NAc-VTA and other brain reward regions) such as: Induction of the transcription factor ΔFosB (sensitization) in NAc Activation of CREB (camp response element-binding protein) in NAc Cocaine psychosis Seizures Movement disorders Schizophrenia Depression Chronic effects of cocaine 2 Majority of health problems associated with a drug abusing lifestyle/ addiction: Addiction dominates life Poor health (malnutrition) Drug injectors are susceptible to AIDS Polydrug abuse Snorting cocaine leads to thining of septum nasal septal perforation Intravenous drug abuse vasculitis, myocarditis,cerebral infarction and infection (HIV, Hep B and C) Cardiac complications are the commonest cause of death (Chest pain, myocardial ischemia and infarction, cardiac dysrhthmias and sudden death) 2
3 Tolerance and dependence Repeated use can lead to tolerance Cross-tolerance can also be a problem Severe psychological, but not physical, dependence Not many drug treatments for cocaine dependence Prolonged behavioural treatments main approach Synthetic products Amphetamines Amphetamine+ its active dextroisomer (dextroamphetamine)+ methamphetamine and methylphenidate very similar pharmacological properties Methamphetamine is the most popular abused drug Street name for synthetic stimulants including amphetamines speed Taken as oral capsules/ intravenously Pharmacokinetics of Amphetamine Readily absorbed from the gut Gradual increase in drug concentration peaks after 1 hour Injection immediate rush or hit Crosses the brain-blood barrier easily Half is excreted unchanged in the urine Acidity/ flow of urine determines half-life Rest metabolised in the liver Mechanism of action of Amphetamine Amphetamine has threefold mode of action: Causes dopamine and noradrenalin to leak into the synaptic cleft Boosts the amount of transmitter released during an action potential Inhibits the reuptake of neurotransmitter into presynaptic vesicles Effect of amphetamine on the mesolimbic reward pathway 3
4 Pharmacological actions of amphetamines I The main central effects of amphetamines are: Locomotor stimulation Euphoria and excitement Intravenous injection orgasmic Increased confidence Hyperactive Talkative Reduction of fatigue Stereotyped behaviour Pharmacological actions of amphetamines II Peripheral symapthomimetic actions: Increased blood pressure Inhibition of gastrointestinal motility Withdrawal leads to: Prolonged sleep Fatigue Depression Anxiety Increased appetite Chronic effects of amphetamines Psychosis Paranoid hallucination state Start 7min-34 hours post drug abuse Neurotoxicity Damage to dopaminergic and serotonergic axons Mehamphetamine associated neurotoxicity in striatum correlates with psychotic symptoms, memory deficits and impaired psychomoter coordination Cardiovascular complications Coronary heart disease Cardiomyopathy/ left ventricular dysfunction Hypertension stroke and cerebral haemorrhage Clinical use of amphetamines Methylphenidate used in treatment of attention deficit-hyperactivity disorder (ADHD) Treatment of Narcolepsy Appetite suppressant Tolerance and dependence Repeated use tolerance Cross tolerance Repeated use over the course of few days amphetamine psychosis Dependence as a consequence of the unpleasant after effects No physical withdrawal Caffeine (1,3,7- trimethylxanthine) World s most popular psychoactive drug Contained in tea, coffee, chocolate, soft drinks, cold relief tablets, headache pills, etc Average cup of strong tea 50-70mg and coffee 170mg of caffeine Average daily consumption in a moderate drinker mg of caffeine each day 4
5 Pharmacokinetics of Caffeine Efficiently absorbed from the GI tract Rapidly distributed in the organism 30-60mins for peak plasma time 60mins before psychoactive properties detected Half life 3-7 hours Lethal concentration in blood 500μM 300mg of caffeine (3 cups of coffee) peak blood concentration of 30μM lipolysis glycerol and free fatty acid levels in the blood plasma Dilates blood vessels and increases urine volume metabolised in liver (Cytochrome P450 1A2) Relaxes smooth muscles of the bronchi, and is used to treat asthma Mechanisms of action of caffeine Does not directly alter catecholamine activity Exerts effect by: Blockade of adenosine receptors (A1 and A2a) Inhibition of phosphodiesterases Mobilization of Ca2+ from intracellular stores Adenosine has inhibitory effects in central/peripheral nervous systems Mechanisms of action of caffeine II Effect of caffeine on A1 receptors A1 receptor distribution hipocampus, cerebellum and cerebral cortex A1 receptors located on presynaptic nerve terminals inhibit release of neurotransmitters Antagonism of A1 receptors by caffeine blockade of the inhibitory effect of adenosine increased cortical/ hippocampal activity vigilance/ information processing/ arousal Mechanisms of action of caffeine III Effect of caffeine on A2a receptors A2a receptor distribution striatum, tuberculum olfactorium A2a receptors located postsynaptically co-expressed with enkephalin and dopamine D2 receptors in striatal neurons Activation of A2a receptors decrease in the affinity of dopamine binding to D2 receptors Antagonism of A2a receptors by caffeine Increase in the potency of endogenous dopamine at D2 receptors enhancement of dopaminergic neurotransmission behavioural effects 5
6 Psychobiological effects: Normal dose Increased arousal Greater alertness Reduction of fatigue Improved performance at motor tasks Improved mental performance No euphoria High dose Insomnia Increased nervousness/ tension/ jitteriness/ irritability Peripheral effects: Coronary artery vasodilator & bronchodilation (smooth muscle relaxer) Increase HR (striated muscle constrictor) Constricts cerebral arteries Acts as diuretic (Gotta go pee) Unwanted side effects of caffeine Indigestion, palpitations, tremor, insomnia, headache Conflicting data on reproductive effects May slow growth in utero, especially high dose Caffeine may be harmful prior to conception May increase the risk of spontaneous abortion > 4 cups/day Osteoporosis Cholesterol increases Tolerance and dependence Tolerance to some effects of caffeine is seen Caffeine is a reinforcing agent Reinforcing effects due to desirable acute stimulatory effect/ undesirable withdrawal symptoms Withdrawal symptoms fatigue, headache, apathy and drowsiness Key references Parrott, A et al (2007) Drugs and behaviour. John Wiley & Sons Ltd. Rang, H.P., Dale, M.M. (2007) Pharmacology. 6 th ed. Churchill Livingstone. Waller, D.G. et al (2007) Medical pharmacology and therapeutics. 2 nd ed. Elsevier Saunders. Fisone, G. et al (2004) Caffeine as a psychomotor stimulant: mechanism of action. CMLS.61: Fredholm, B.B. et al (1999) Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacological Reviews. 51: 83 White, S.M & Lambe, C.J.T. (2003) The pathophysiology of cocaine abuse. Journal of Clinical Forensic Medicine 10:
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