<unk> s can be subdivided based on their activity on the central nervous system, compounds with hallucinogenic properties are the MDMA-related compounds. All<unk>  acts as psychostimulants, which produce<unk> ory effects and leads to hyperarousal and increased movement. While MDMA-related compounds possess a structure similar to mescaline and has hallucinogenic properties on top of psychostimulant properties.<unk>  facilitates monoamine neurotransmission by blocking membrane monoamine transporters, which results in inhibited clearance of monoamine. Examples of monoamine transporters include dopamine transporters, norepinephrine transporters and serotonin transporters.<unk>  are also competitive antagonists that compete with the monoamine neurotransmitters due to their similar structures.<unk>  then enter the presynaptic neuron and inhibit the vesicular monoamine transporter 2 (VMAT2) to reduce the reuptake of monoamine neurotransmitters.<unk>  inhibits monoamine oxidase and hence inhibits monoamine degradation and some of them may have interaction with presynaptic intracellular receptors that promote monoamine neurotransmission. For instance, methamphetamine acts as an agonist of sigma-1 receptor. Pharmacodynamics<unk>  use disorders are related to the GABA system. Research shows that<unk>  use would affect normal function of the GABAA receptors. Clonazepam, which is a GABAA receptor agonist, is shown to prevent the acquisition of behavioural sensitization to methamphetamine. GABAA receptor antagonist is shown to aggravate<unk>  use disorders. Hence, a possible mechanism could be that activating GABAA receptor reduces dopaminergic neurotransmission and GABAA receptors may have an inhibitory role in<unk> -induced disorders.<unk>  also inhibit GABAB receptors, glutamic acid decarboxylase (GAD), GABA transporters (GAT) and promote GABA metabolism. This leads to the reduced expression of extracellular GABA expression, inhibited biosynthesis of GABA-nergic neurotransmitter and depressed function of GABAB receptors-GIRK channels. Pharmacokinetics<unk>  can be administered via oral (swallowing), intranasal (inhaling vapour or snorting), and intravenous routes. Taking<unk>  orally is the most common route of administration. The response time and other pharmacokinetics profile of<unk>  varies for different routes of administration. +Clinical pharmacokinetics of methamphetamine Route Dose Bioavailability Cmax (g/l) Tmax (minutes) T1/2 (hours) Time to peak effect (minutes) Intravenous 30 mg 100% 108 22 6 9.1 0.8 15 Oral 30 mg 67% 94.1 216 9.1 18 2 Smoking 30 mg 67%/ 90 10% 47 6 150 30 12 1 180 Intra-nasal 50 mg 79% 113 8 169 8 11 1 15<unk>  are metabolised by liver enzymes especially cytochrome P450 2D6, producing metabolites including 4-hydroxyamphetamine, 4 hydroxynorephedrine, hippuric acid, benzoic acid and benzyl methyl ketone. The metabolism of<unk>  may vary from person to person due to genetic polymorphism of the enzyme CYP450 2D6. Under normal conditions, around 5 to 30% of amphetamine is excreted unchanged in the urine. However, the urinary excretion of amphetamine and other<unk>  is highly dependent on the pH. A small amount of amphetamine is also produced from metabolism of methamphetamine, but does not cause any significant clinical effect.
Amphetamine type stimulant
Atypical antidepressant
Antipsychotic ester
Substituted amphetamine
Heterocyclic antidepressant
Synthetic cannabinoids
Tetracyclic antidepressant
Tricyclic antidepressant