What is the difference between what cocaine and amphetamine microinjections into the nucleus accumbens do to animals?
Amphetamine microinjections have a reinforcing effect, whereas cocaine microinjections don’t.
What family is amphetamine part of?
Synthetic psychostimulants related to dopamine.
Name the synthetic psychostimulants.
Amphetamine, methamphetamine, ephedrine, cathinone, MDMA, MDA, MDE.
Which synthetic psychostimulants have been used in plant form?
Cathinone - khat.
Ephedrine - ephedra vulgaris, a herbal remedy.
What dopamine pathway does amphetamine primarily affect?
The nigrostriatal pathway.
What have been the uses of ephedra?
- It was used as a herbal remedy for 5000 years, as it decreases appetite and provides a feeling of heightened energy.
- Was used as an appetite suppressant (now banned)
- Used for asthma in 1920s, led to amphetamine inhaler
- Later marketed for narcolepsy.
What is pseudoephedrine used for?
As a bronchodilator.
What is amphetamine used to treat?
ADHD - Ritalin.
What do amphetamines do on a neuronal level?
- They’re indirect dopamine agonists
- At high doses they inhibit catecholamine metabolism by monoamine oxidase (MAOA)
- Reverse dopamine transporters = extra release and no reuptake, also provokes release
- Also noradrenaline release
Which is stronger out of amphetamine and methamphetamine?
What is the elimination half-life of amphetamine?
7-30 hours, but some users take repeated IV injections every few hours over a period of days.
What did Griffith et al (1972) do?
Gave 7 pts (users w/no history of psychosis) dextroamphetamine every hour for up to 5 days.
What did Griffth et al (1972) find?
All the participants became psychotic within 2-5 days, with delusions mostly auditory but also included poisoning by the experimenters and electric dynamo thought control.
What is dextroamphetamine commonly known as?
What are the adverse effects of amphetamines?
- Psychotic reactions (delusional beliefs, methamphetamine violence and flashbacks).
- Neurotoxicity (reduced TH, DA and DAT density, ecstasy affects 5-HT).
What could amphetamine use predispose a user to?
Developing Parkinson’s - same reduction of DAT in striatum, which is progressive.
MDMA is known as the _____ amphetamine.
Entactogenic. It’s supposed to elicit an enhanced ability to introspect.
What psychological effects does MDMA produce?
Mild euphoria, enhanced sensory perception, increased energy, feelings of well-being and confidence, a desire to be with people and sexual arousal.
What did McCann et al (1998) find?
Reduced striatal DAT binding in abstinent drug users and PD.
What physiological effects does MDMA produce?
Increased HR, temp and BP, sweating, salivation, tremor, trismus and bruxism.
What is trismus?
Tightening of the jaw muscles.
What is bruxism?
What is MDMA’s primary mode of action?
It enhances the release and prevents re-uptake of serotonin - it’s an indirect 5-HT agonist.
When was MDMA first developed and used?
1914, used therapeutically in the 1970s, made illegal in 1985.
What neurotransmitter, apart from serotonin, does MDMA stimulate release of?
What is the main issue with repeated MDMA exposure?
It damages serotonergic pathways in the brain (Boot et al, 2000).
Pruning of serotonergic axons and terminals in cortex and hippocampus. Some abnormal reinnervation.
What effects do amphetamines have on cue conditioning/associative learning?
According to Norman and Cassaday (2003), amphetamines increase CS salience in various procedures (latent inhibition, overshadowing, trace conditioning and contextual conditioning).
What are the different treatment options for amphetamine addiction?
- Pharmacological (DA antagonists)
- Behavioural (avoid triggers, counterconditioning)
- Psychosocial (counselling, CBT and cue exposure)
What did Kuczenski and Segal (2002) do?
Gave adolescent rats Ritalin (or saline), reduced activity - treatment for ADHD (theory is that dopamine system is underactive).
What is methylphenidate?