amphetamines Flashcards
what is amphetamine?
- a CNS stimulant
- makes messages between brain and body move faster
- often used to treat ADHD
are mild/moderate effects of amphetamines typically positive or negative?
positive
identify some positive mild/moderate effects of amphetamines
- euphoria (positive mood)
- heightened energy
- increased flow of ideas
- inflated self-esteem
identify some negative mild/moderate effects of amphetamines
- dysphoria (negative mood)
- insomnia
- restlessness
- mild anorexia
are sever effects of amphetamines typically positive or negative?
(almost entirely) negative
identify some severe effects of amphetamines
- irritability
- hostility
- anxiety
- compulsive motor stereotypes
- rambling
- inherent speech
- delusions of grandiosity (believing you have special powers)
identify an important distinction between using cocaine vs amphetamine microinjections on the role of nucleus accumbens
amphetamines are reinforcing when microinjected directly into nucleus accumbens
how are amphetamines related to psychomotor stimulants?
- psychomotor stimulants = drugs that act on CNS to increase alertness
- amphetamines are a family of synthetic psycho-stimulants
- all these are structurally related to dopamine (DA)
- MDMA (ecstasy) is part of amphetamine family
identify some naturally occurring substances that are included in the amphetamine family
- ephedrine (from ephedra plant)
- cathinone (from khat)
what are some uses of ephedra?
- appetite suppressant (now banned)
- treat asthma (amphetamine inhaler)
- used to treat narcolepsy
outline Kuczenski & Segal (2002) study into psychomotor stimulants and ADHD
- studied adolescent rats in the active phase of their cycle
- injected rats with: saline solution (control), 0.75mg methylphenidate (MP), 1.0mg MP
- activity levels decreased
- usually treatment with amphetamines normally increase activity
- However, at low doses and in juvenile rats there was paradoxical reduction in activity
describe the pharmacology of amphetamine
- amphetamine is an indirect agonist of dopamine
- high dose MAOI
- affects noradrenaline
what is meant by ‘amphetamine is an indirect agonist of dopamine’?
- agonist = a substance that initiates a response when combined with a receptor
- amphetamine is taken up by dopamine transporters
- enters neuron terminal
- when amphetamine is inside terminal -> stimulates release of dopamine
- increases dopamine availability in synaptic cleft
- activity in post-synaptic cleft dopamine neurones = increased
what is meant by ‘high dose MAOI’?
- at high doses, amphetamine acts as monoamine oxidase inhibitor
- means reduces enzymatic breakdown of dopamine and noradrenaline
what is meant by ‘[amphetamine] affects noradrenaline’?
- amphetamine has additional affects on noradrenaline
- this is due to amphetamine entering noradrenaline neurones
- this increases noradrenaline release
- effects PNS to increase heart rate an blood pressure via adrenoreceptors
what is meant by ‘half-life of 7-30 hours’?
- elimination half-life of amphetamine = 7-30 hours
- means user should notice significant reductions in its effects within 24 hours of ingestion
what effect does administering amphetamines by IV?
- intra-venous injections = IV -> directly into bloodstream
- known to result in sensitisation
- this further increases dopamine effects
outline the mechanisms of amphetamine-stimulated DA release
- amphetamine taken up by dopamine active transporter
- inside dopamine active transporter provokes the dopamine release
- dopamine active transporter also functions in reverse to further release dopamine
outline Griffith et al. (1972) study into amphetamine psychosis
- development of psychotic symptoms seen in heavy users
- studied 7 ppts
- ppts had history of using drugs, but no history of psychosis
- they were given 10mg of dextroamphetamine (amphetamine) every hour for up to 5 days
FINDINGS
- found all ppts became psychotic within 2-5 days
- delusions mostly auditory, electric dynamo thought control, poisoning by experimenters
identify adverse effects of amphetamines
in high doses
- PSYCHOTIC REACTIONS
- NEUROTOXICITY
identify psychotic reaction to amphetamines
- delusional beliefs
- methamphetamine with violence
- methamphetamine with flashbacks
identify neurotoxicity example as consequence to using amphetamines
- damage to dopamine system
shown in reduced density of dopamine transporter - damage to serotonergic (5-HT) system
shown in reduced fibre density (especially in ecstasy use)
outline McCann et al. (1998) study into the damage of the brain from amphetamine use
- studied abstinent drug users
- dopamine transporter illustrated using radio-labelled cocaine
- allowed imaging technique (PET scan) could be used to map changed of dopamine transporter
- change was shown by reduced binding of radio-labelled cocaine
FINDINGS
- study shows visualisation of damage to striatum of brain
- damage similar to whats seen in Parkinson’s disease
when was MDMA (ecstasy) developed
1914
what is MDMA an indirect agonist of?
5-HT
what does MDMA being an indirect agonist of 5-HT result in?
neurotoxic damage
outline Hatzidimititriou et al. (1999) study into reduced serotonergic (5-HT) function in neocortex after MDMA
- studied squirrel monkeys that had been treated with MDMA
- monkeys were given 5mg of MDMA twice daily for 4 days
- fibres were stained white
- monkeys then killed 2 weeks later or 7 years later
FINDINGS
- evidence for reduced 5-HT function
- across 3 different cortical regions (frontal, parietal, visual)
- 5-HT fibres were stained white
- effects of MDMA damage still present 7 years after study
what effects does amphetamine have on cue conditioning?
- associative learning is increased under amphetamines
learning usually weaker:
- when cues have been exposed previously (latent inhibition)
- when there is alternative cue competing for attention (overshadowing procedures)
- when there is delay in time between cue and outcome (trace conditioning
- when learning cues are provided by context from environment (contextual conditioning)
- when treatment of amphetamine used –> enhances conditioning cues (these would usually be disregarded
what does increased cue salience have implications for?
cue salience = how noticeable a cue is to the individual
- implications for treatment
- important due to fewer pharmacological approaches have tested for amphetamines
- if you can block the hyper-attention, should be able to reduce development of triggers associated with drug taking
how does the pharmacological approach treat amphetamine addiction with those who used cocaine?
- use dopamine antagonists
how does the behavioural approach treat amphetamine addiction with those who used cocaine?
- avoid triggers for relapse
- using ‘counter-conditioning’
- i.e.: a cue producing a conditioned incentive effect paired with an aversive stimulus
how does the psychosocial approach treat amphetamine addiction with those who used cocaine?
- counselling
- CBT
- cue exposure
- aim to reduce stress which influences how responsive the dopamine system is
what does cocaine tolerance depend on?
- administration schedule
- behavioural response measured
- time elapsed since last dose
- if short time since last dose, you build tolerance
- if long time since last dose, you build sensitisation
