Top Gene Interactions
- Metabolism: Hepatic Half Life: 10 hours
- Uses/Sources: For treatment of Attention Deficit Disorder with Hyperactivity (ADDH) and narcolepsy in children.
- Health Effects: Prolonged use may cause hallucinations and intense paranoia. Amphetamines are psychologically addictive. Users who stop using them report that they experience various mood problems such as aggression and anxiety and intense cravings for the drugs. Using large amounts of these drugs can result in a condition known as amphetamine psychosis -- which can result in auditory, visual and tactile hallucinations, intense paranoia, irrational thoughts and beliefs, delusions, and mental confusion.
- Symptoms: The most common presenting symptoms seen are agitation, hallucinations, suicidal behaviour, and chest pain.
- Treatment: Management of acute amphetamine intoxication is largely symptomatic and includes gastric lavage, administration of activated charcoal, administration of a cathartic and sedation. (L1712)
- Route of Exposure: Oral. Amphetamine forms easily absorbed molecules that are highly lipid soluble.
- Carcinogenicity: No indication of carcinogenicity to humans (not listed by IARC).
- Toxicity: LD50: 180 mg/kg (Subcutaneous, Rat) (A308)
Mechanism of Action
|Target Name||Mechanism of Action||References|
Beta adrenergic receptor
Synaptic vesicular amine transporter
5-hydroxytryptamine receptor 1A
Amine oxidase [flavin-containing] B
Sodium-dependent noradrenaline transporter
D(1A) dopamine receptor
Sodium-dependent serotonin transporter
Alpha adrenergic receptor
D(2) dopamine receptor
Trace amine-associated receptor 1
Cocaine- and amphetamine-regulated transcript protein
Sodium-dependent dopamine transporter
Alpha-2A adrenergic receptor
Alpha-1A adrenergic receptor
|Amphetamines stimulate the release of norepinephrine from central adrenergic receptors. At higher dosages, they cause release of dopamine from the mesocorticolimbic system and the nigrostriatal dopamine systems. Amphetamine may also act as a direct agonist on central 5-HT receptors and may inhibit monoamine oxidase (MAO). In the periphery, amphetamines are believed to cause the release of noradrenaline by acting on the adrenergic nerve terminals and alpha- and beta-receptors. Modulation of serotonergic pathways may contribute to the calming affect.||