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Cocaine
typically snorted (mucus membrane) in powder form or smoked (quick at entering bloodstream) in its free-base form (crack)
Reaches peak in blood at 30-60 minutes
Easily penetrates the blood brain barrier (lipophilic)
Biological half life = 30-90 minutes - leaves body relatively quickly but depends on how much fat you have, tolerance etc
Cocaine short term effects
is a stimulant so increases:
euphoria
Energy
Confidence
Talkativeness
Activity
Alertness
Attention
Action of cocaine at mono-aminergic synapses
mono-amines: serotonin, dopamine, noradrenaline/ norepinephrine (suppresses arousal and plateau) and Adrenalin/ epinephrine
Cocaine blocks reuptake (recycle neurotransmitters back into presynaptic neuron so there’s less in the synapse) from occurring so neurotransmitters stay for longer in the synapse → longer affect
Autoreceptor
Signal to presynaptic terminal to not release anymore neurotransmitters if there are too many in the synapse
Cocaine long term effects
lack of reuptake/ recycling → depletion of monoamines as recycling tends to be a faster process than making neurotransmitters → lower levels in the presynaptic terminal → crash into depression after several hours (lack of serotonin)
Remedied by taking more cocaine → 2-3 day cocaine binges
Destruction of the nasal septum due to restricted blood flow
Schizophrenia type symptoms due to too much dopamine e.g. hallucinations, delusions of persecution, mood disturbances and repetitive behaviours
Sexual dysfunction
Tolerance to the desired effects (from noradrenaline and serotonin) so need higher dose
Sensitisation (low dose required) to achieve negative effects e.g. convulsiveness, stereotyped behaviour and addictiveness (from dopamine)
Cocaine addictiveness
direct effect on dopamine released in the nucleus accumbens and PFC → direct activation of seeking and reward pathways
Strong psychological (dopamine) addictiveness but much less physical addictiveness (withdrawal)
Action of amphetamines at mono-aminergic synapses
same as cocaine
Reverse reuptake channels so they’re pushing the neurotransmitters back into the synapse (reverse effect)
Ritalin (methylphenidate)
acts similarly to cocaine by blocking the mono-amine re-uptake transporter → gradual releases so doesn’t have the same immediate effect as cocaine
Effective treatment for attention deficit hyperactivity disorder (ADHD)
Caffeine
typically ingested in coffee/ soft drinks
Concentration peaks after ~40 mins
Easily passes through the blood brain barrier
Biological half life = 3.5-5 hours (longer in children)
Lethal dose = 100 cups of coffee (10g of caffeine)
Caffeine short term effects
psychostimulant
Increases alertness and wakefulness
Clear thinking
Restlessness
Difficulty with fine movements (shaky hands)
Increases cardiac contractions
Constricts blood vessels
Caffeine side effects
anxiety
Insomnia
Change in mood
Hypertension
Caffeine physiological action
blocks adenosine receptors which is involved in sleep and vasodilation (blood vessels)
Stimulates adrenaline release from adrenal medulla
Caffeine long term effects
sleep deprivation (especially slow wave)
Can be countered by using more caffeine to wake up in the morning → dependence
Caffeine addictiveness
physical dependence/ withdrawals symptoms include:
headaches (vasodilation)
Sleepiness
Irritability
Difficulty concentrating
Psychological dependence: increases dopamine released in nucleus accumbens
Nicotine
from the tobacco leaf
Typically smoked/ vaped (quick way of entering the bloodstream) or sometimes chewed
Within 7 seconds of a puff, 25% nicotine in the smoke has crossed the blood brain barrier
Biological half life of 2 hours in a chronic smoker → regular intakes to avoid withdrawal
Nicotine short term effects
induces vomiting - affects brain stem area involved in vomiting - regular smokers will get tolerance to this
Reduces muscle tone (relaxes) so withdrawal → tense muscles
Reduces weight gain so withdrawal → weight gain
Increases heart rate and blood pressure
Nicotine physiological action
Binds to nicotine acetylcholine receptors found in the brain which are involves in stimulation of the sympathetic nervous system including release of adrenaline from the adrenal gland
Also acts on parasympathetic nervous system but influences the sympathetic
Agonist
Nicotine long term effects
tolerance
Wears out the heart more quickly
The major problems come from other components of tobacco/ cigarette smoke (cancer, cardiovascular disease etc) but nicotine causes addiction
Nicotine addictiveness
physical dependence/ withdrawals include:
craving
Irritability
Increased appetite
Insomnia
Argued to be the most addictive drug psychologically due to its effect on dopamine in nucleus accumbens being so high
70% smokers become addicted (Compared to 30% heroin users)
20% who quit stay quit after 2 years - perhaps due to how addictive it is and how easy it is to access
Alcohol
usually ingested (drink)
Reaches max blood concentration in 30-90 minutes = quick but depends on how full you are (more food = slower)
Easily crosses blood brain barrier (soluble in both water and lipids)
Mostly eliminated by the liver which breaks it down at a steady rate
Alcohol short term effects
low dose = mild euphoria and anxiolytic (lowers anxiety) = easier to interact with others
Higher dose = intoxication:
slower reflexes
In coordination
Sedation
Memory problems
Dilation of blood vessels as skin is warm due to more blood → felling less cold but causes core temperature to lower → heat loss
Alcohol physiological action
agonist (mimics affect) of GABA-A receptors which increases inhibitory processes → more sleepy
Antagonist (block effects) of NMDA (involved in memory) receptors e.g. glutamate which suppresses excitatory processes → inability to form new memories
Alcohol long term affects
cirrhosis/ failure of the liver
Brain damage, especially to the hippocampus → Korsakoff’s syndrome = permanent inability to make new memories
Alcohol addictiveness
physical dependence/ withdrawal:
tolerance induced even from one night of drinking → mild withdrawal symptoms (hangover)
Chronic use → strong withdrawal symptoms which can be fatal e.g. delirium tremens which is where there is not enough inhibition due to raised GABA during alcohol intake naturally lowers levels over time → seizures due to overactive cells. Can be stabilised over time if no alcohol is consumed
Psychological dependence:
increases dopamine release in the nucleus accumbens
Strong heritable component to alcoholism