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PSGY1005 Addiction and the Brain > amphetamines > Flashcards

amphetamines Flashcards

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1
Q

what is amphetamine?

A
  • a CNS stimulant
  • makes messages between brain and body move faster
  • often used to treat ADHD
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2
Q

are mild/moderate effects of amphetamines typically positive or negative?

A

positive

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3
Q

identify some positive mild/moderate effects of amphetamines

A
  • euphoria (positive mood)
  • heightened energy
  • increased flow of ideas
  • inflated self-esteem
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4
Q

identify some negative mild/moderate effects of amphetamines

A
  • dysphoria (negative mood)
  • insomnia
  • restlessness
  • mild anorexia
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5
Q

are sever effects of amphetamines typically positive or negative?

A

(almost entirely) negative

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6
Q

identify some severe effects of amphetamines

A
  • irritability
  • hostility
  • anxiety
  • compulsive motor stereotypes
  • rambling
  • inherent speech
  • delusions of grandiosity (believing you have special powers)
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7
Q

identify an important distinction between using cocaine vs amphetamine microinjections on the role of nucleus accumbens

A

amphetamines are reinforcing when microinjected directly into nucleus accumbens

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8
Q

how are amphetamines related to psychomotor stimulants?

A
  • 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
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9
Q

identify some naturally occurring substances that are included in the amphetamine family

A
  • ephedrine (from ephedra plant)
  • cathinone (from khat)
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10
Q

what are some uses of ephedra?

A
  • appetite suppressant (now banned)
  • treat asthma (amphetamine inhaler)
  • used to treat narcolepsy
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11
Q

outline Kuczenski & Segal (2002) study into psychomotor stimulants and ADHD

A
  • 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
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12
Q

describe the pharmacology of amphetamine

A
  • amphetamine is an indirect agonist of dopamine
  • high dose MAOI
  • affects noradrenaline
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13
Q

what is meant by ‘amphetamine is an indirect agonist of dopamine’?

A
  • 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
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14
Q

what is meant by ‘high dose MAOI’?

A
  • at high doses, amphetamine acts as monoamine oxidase inhibitor
  • means reduces enzymatic breakdown of dopamine and noradrenaline
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15
Q

what is meant by ‘[amphetamine] affects noradrenaline’?

A
  • 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
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16
Q

what is meant by ‘half-life of 7-30 hours’?

A
  • elimination half-life of amphetamine = 7-30 hours
  • means user should notice significant reductions in its effects within 24 hours of ingestion
17
Q

what effect does administering amphetamines by IV?

A
  • intra-venous injections = IV -> directly into bloodstream
  • known to result in sensitisation
  • this further increases dopamine effects
18
Q

outline the mechanisms of amphetamine-stimulated DA release

A
  • 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
19
Q

outline Griffith et al. (1972) study into amphetamine psychosis

A
  • 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
20
Q

identify adverse effects of amphetamines

A

in high doses
- PSYCHOTIC REACTIONS
- NEUROTOXICITY

21
Q

identify psychotic reaction to amphetamines

A
  • delusional beliefs
  • methamphetamine with violence
  • methamphetamine with flashbacks
22
Q

identify neurotoxicity example as consequence to using amphetamines

A
  • 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)
23
Q

outline McCann et al. (1998) study into the damage of the brain from amphetamine use

A
  • 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
24
Q

when was MDMA (ecstasy) developed

A

1914

25
Q

what is MDMA an indirect agonist of?

A

5-HT

26
Q

what does MDMA being an indirect agonist of 5-HT result in?

A

neurotoxic damage

27
Q

outline Hatzidimititriou et al. (1999) study into reduced serotonergic (5-HT) function in neocortex after MDMA

A
  • 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

28
Q

what effects does amphetamine have on cue conditioning?

A
  • 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
29
Q

what does increased cue salience have implications for?

A

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
30
Q

how does the pharmacological approach treat amphetamine addiction with those who used cocaine?

A
  • use dopamine antagonists
31
Q

how does the behavioural approach treat amphetamine addiction with those who used cocaine?

A
  • avoid triggers for relapse
  • using ‘counter-conditioning’
  • i.e.: a cue producing a conditioned incentive effect paired with an aversive stimulus
32
Q

how does the psychosocial approach treat amphetamine addiction with those who used cocaine?

A
  • counselling
  • CBT
  • cue exposure
  • aim to reduce stress which influences how responsive the dopamine system is
33
Q

what does cocaine tolerance depend on?

A
  • 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

PSGY1005 Addiction and the Brain (18 decks)

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