Amphetamine type stimulant

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Amphetamine type stimulants (ATS) are a group of synthetic drugs that are chemical derivatives of the parent compound alpha-methylphenethylamine, also known as amphetamine. Common ATS includes amphetamine, methamphetamine, ephedrine, pseudoephedrine, 3,4-methylenedioxymethamphetamine (MDMA), 3,4-methylenedioxyamphetamine (MDA) and 3,4-methylenedioxyethylamphetamine (MDEA). [1] ATS when used illicitly has street names including ice, meth, crystal, crank, bennies, and speed. Within the group of amphetamine-type stimulants, there are also prescription drugs including mixed amphetamine salts, dextroamphetamine, and lisdexamfetamine.

Contents

Amphetamine was first synthesized in 1887 by the Romanian chemist Lazar Edeleano. [2] [3] It has since been used to treat a range of disorders from asthma to ADHD and illicitly for recreational purposes. Amphetamine-type stimulants contain chemical groups including unsubstituted phenyl ring, a methyl group at the alpha-position, and primary amino group, which accounts for its psychostimulant activities. ATS with multiple substitutions on the phenyl ring has a hallucinogenic effect on top of the psychostimulant effect, and are categorised as the ecstasy-class drugs. [4]

Amphetamine-type stimulants in general are sympathomimetic amine that stimulates the central nervous system, also proven to cause insomnia, arousal, and reduced hunger. Due to its physiological and psychological effects, ATS has been used to suppress appetite, improve cognitive performance, as well as treating ADHD, depression, and narcolepsy. Amphetamine type stimulants are also known for their addictive property and widespread problem of substance abuse. The adverse effects of ATS, especially when chronically used, include obsessive–compulsive tendencies, anxiety, paranoia, hallucinations, aggression, mania and in extreme cases, amphetamine psychosis.

History

Amphetamine, the parent compound of amphetamine-type stimulants was first synthesized by Romanian chemists Lazar Edeleano in 1887. Around the same time, amphetamine's precursor ephedrine was also abstracted from a Chinese herbal medicine ephedra by a Japanese Chemist. [5] After its discovery, amphetamine was purified and put into medical use in the 1900s. [5] Amphetamine was originally sold as a decongestant inhaler in the United States in 1933 and led to widespread ATS abuse in military forces and civilians later on. [5]

The details of history of amphetamine can be found here.

Chemistry

Ephedrine is the precursor of synthetic amphetamines. The diastereomer of ephedrine, pseudoephedrine is found in Ephedra sinica together along with ephedrine. Ephedrine and pseudoephedrine are both generally used for weight reduction and performance enhancement. They can also be reduced to methamphetamine. [2]

The activity of amphetamine-type stimulants depends on their unsubstituted phenyl ring, alphy methyl group, primary amino group and two-carbon side-chain that connects the primary amino group and the phenyl ring. [6]

Hallucinogenic activity of ATS are often caused by multiple substitutions on the phenyl ring, examples include 4-bromo-2,5-dimethoxyamphetamine and 2,5-dimethoxy-4-methylamphetamine. When the methoxy group is substituted in the para position of the ATS molecule, the hallucinogenic potency will become significantly high. [6]

Pharmacology

Amphetamine type stimulants can be subdivided based on their activity on the central nervous system, compounds with hallucinogenic properties are the MDMA-related compounds. All ATS act as psychostimulants, which produce stimulatory effects and lead to hyperarousal and increased movement [7] , while MDMA-related compounds that possess a structure similar to mescaline have hallucinogenic properties on top of psychostimulant properties. [1]

ATS 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. [1]

ATS are also competitive antagonists that compete with the monoamine neurotransmitters due to their similar structures. ATS then enter the presynaptic neuron and inhibit the vesicular monoamine transporter 2 (VMAT2) to reduce the reuptake of monoamine neurotransmitters. [1]

ATS inhibits monoamine oxidase and hence inhibits monoamine degradation and some of them may have interaction with presynaptic intracellular receptors that promote monoamine neurotransmission. [1] For instance, methamphetamine acts as an agonist of sigma-1 receptor. [8]

Pharmacodynamics

ATS use disorders are related to the GABA system. Research shows that ATS use would affect normal function of the GABAA receptors. [9] 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 ATS use disorders. Hence, a possible mechanism could be that activating GABAA receptor reduces dopaminergic neurotransmission and GABAA receptors may have an inhibitory role in ATS-induced disorders. [9] [10]

ATS 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. [10]

Pharmacokinetics

ATS can be administered via oral (swallowing), intranasal (inhaling vapour or snorting), and intravenous routes. Taking ATS orally is the most common route of administration. [11] The response time and other pharmacokinetics profile of ATS varies for different routes of administration.

Clinical pharmacokinetics of methamphetamine [12]
RouteDoseBioavailabilityCmax (g/L)Tmax (minutes)T1/2 (hours)Time to peak effect (minutes)
Intravenous30 mg100%108 2269.1 0.815
Oral30 mg67%94.12169.118 2
Smoking30 mg67%/ 90 10%47 6150 3012 1180
Intra-nasal50 mg79%113 8169 811 115

ATS are metabolised by liver enzymes especially cytochrome P450 2D6, producing metabolites including 4-hydroxyamphetamine, 4 hydroxynorephedrine, hippuric acid, benzoic acid and benzyl methyl ketone. [13] The metabolism of ATS may vary from person to person due to genetic polymorphism of the enzyme CYP450 2D6. [13] Under normal conditions, around 5 to 30% of amphetamine is excreted unchanged in the urine. [14] However, the urinary excretion of amphetamine and other ATS 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. [12]

Uses

Treatment of Attention Deficit Hyperactivity Disorder

Dextroamphetamine and lisdexamfetamine are widely used for Attention Deficit Hyperactivity Disorder (ADHD). [15] These two drugs are first-line drugs for children, adolescents and adults. [16]

Antidepressant

Amphetamine has been used in the past to treat anhedonia, a major phenomenon of depression. The use of ATS as an antidepressant was no longer common after the production of the more effective tricyclic antidepressants and monoamine oxidase inhibitors (MAOI). ATS were established as a detriment to public health. [5]

Appetite suppressant

A study conducted by the pharmaceutical company Smith, Kline & French (SKF) in 1947 showed that amphetamine can affect the brain center for appetite and help to reduce weight. In the late 1960s, weight reduction was the most common indication for ATS. [5] Nowadays, to suppress appetite, phentermine is still used. [2]

Treatment for narcolepsy

Amphetamine type stimulants can be used in the treatment of narcolepsy, a rare neurological disorder where the brain is unable to regulate the sleep-wake mechanism. [17] Amphetamines causes an increase in dopamine release, which is the proposed mechanism for its wake-promoting effect. [18] ATS such as dextroamphetamine are used in the treatment of narcolepsy when another CNS stimulant, modafinil is not effective. [19]

Cognitive performance

Early users of amphetamine-type stimulants may report that their cognitive performance and working abilities are improved . Low-to-moderate doses of ATS improves psychomotor output without significantly affecting memory, verbal task performance and intelligence measures. ATS may boost the school performance of some students through emotional mechanisms that increase their confidence. [5] However, amphetamine-type stimulants is not prescribed for this use legally.

Abuse

Amphetamine is frequently used for pleasure and abused because of the addictive properties. The definition of ATS abuse is a maladaptive pattern of substance use manifested by recurrent and significant adverse consequences related to the repeated use of substances. [20] While dependence refers to the use of amphetamine 'accompanied by evidence of tolerance, withdrawal, or compulsive behaviour". [21] Abuse of ATS is a threat to global public health. The United Nations World Drug Report states that about 0.3-1.3% of the global population has ATS abuse problems, where methamphetamine accounts for 71% of global ATS seizures. [22]

Adverse effects

The adverse effect of ATS may be caused by many factors, including overdose of prescribed drugs, or use of illicit substance that are not safe in any pharmacological relevant dose. [23] ATS-related fatality and toxicity usually arises from abuse of ATS, rather than adverse drug reactions. ATS may lead to serious health issues with dose-dependent severity. [23] [4]

Undesired acute effectsEffects of chronic Use

Psychosis

Substantial evidence shows that psychotic patients, especially patients with schizophrenia, are more likely to engage in ATS abuse. ATS abuse inhibits dopamine transporter (DAT) and increases dopamine level in the synaptic cleft. The extent of DAT inhibition is associated with the symptoms. [24] Amphetamine-type stimulants-induced psychosis has been reported ever since 1938. Symptoms mainly include delusions and hallucinations. Different kinds of hallucinations are also seen, like auditory, visual, olfactory and tactile hallucinations. [21] Less common symptoms are bizarre behaviour and thought disorder. Though some believed that the ATS-induced psychosis cannot be distinguished from schizophrenia, [25] delusions of persecution are often reported as a characteristic of ATS-induced psychosis. [21]

The duration of ATS-induced psychosis has substantial variations, from weeks to months. Based on their durations, psychosis can be divided into two types. One type has a shorter psychotic state that shows improvement as the central action of ATS changes. The other type has a longer duration. [21]

Toxicity

The toxic dose of ATS varies between person due to development of drug tolerance and genetic polymorphism of the CYP450 2D6 gene. [13] Different ATS also have different toxic dose. Methamphetamine fatality from ATS have been reported after ingestion of a minimal dose of 1.3 mg/kg, while the estimated minimum lethal dose in a non-addicted adult is 200 mg. [14] [26] Generally, children are more likely to develop toxicity and have lower chances of developing tolerance. [14]

Treatment

Studies suggest treatment of ATS-induced psychosis by risperidone and olanzapine. [24] While some suggest the usage of low-dose antipsychotic medications to alleviate the symptoms by preventing sensitisation. [27]

Studies show that antidepressants like fluoxetine, imipramine and desipramine have very limited effects for ATS abuse since they may reduce craving or increase period of adherence to short-to-medium-term treatments. [28]

A variety of psychosocial interventions have been shown to be effective in reducing substance abuse and risk behaviours associated with ATS. [29] There is a strong recommendation that intensive psychosocial interventions be implemented, developed, and adapted to the social context in which they are implemented

Related Research Articles

<span class="mw-page-title-main">Amphetamine</span> Central nervous system stimulant

Amphetamine is a central nervous system (CNS) stimulant that is used in the treatment of attention deficit hyperactivity disorder (ADHD), narcolepsy, and obesity. Amphetamine was discovered as a chemical in 1887 by Lazăr Edeleanu, and then as a drug in the late 1920s. It exists as two enantiomers: levoamphetamine and dextroamphetamine. Amphetamine properly refers to a specific chemical, the racemic free base, which is equal parts of the two enantiomers in their pure amine forms. The term is frequently used informally to refer to any combination of the enantiomers, or to either of them alone. Historically, it has been used to treat nasal congestion and depression. Amphetamine is also used as an athletic performance enhancer and cognitive enhancer, and recreationally as an aphrodisiac and euphoriant. It is a prescription drug in many countries, and unauthorized possession and distribution of amphetamine are often tightly controlled due to the significant health risks associated with recreational use.

<span class="mw-page-title-main">Psychopharmacology</span> Study of the effects of psychoactive drugs

Psychopharmacology is the scientific study of the effects drugs have on mood, sensation, thinking, behavior, judgment and evaluation, and memory. It is distinguished from neuropsychopharmacology, which emphasizes the correlation between drug-induced changes in the functioning of cells in the nervous system and changes in consciousness and behavior.

<span class="mw-page-title-main">Stimulant</span> Drug that increases activity of central nervous system

Stimulants are a class of drugs that increase the activity of the brain and the spinal cord. They are used for various purposes, such as enhancing alertness, attention, motivation, cognition, mood, and physical performance. Some of the most common stimulants are caffeine, nicotine, amphetamines, cocaine, and modafinil.

<span class="mw-page-title-main">Methylphenidate</span> Central nervous system stimulant

Methylphenidate, sold under the brand names Ritalin and Concerta among others, is a potent central nervous system (CNS) stimulant used medically to treat attention deficit hyperactivity disorder (ADHD) and, to a lesser extent, narcolepsy. It is a primary medication for ADHD ; it may be taken by mouth or applied to the skin, and different formulations have varying durations of effect, commonly ranging from 2-4 hours. For ADHD, the effectiveness of methylphenidate is comparable to atomoxetine but modestly lower than amphetamines.

<span class="mw-page-title-main">Methcathinone</span> Psychoactive stimulant

Methcathinone is a monoamine alkaloid and psychoactive stimulant, a substituted cathinone. It is used as a recreational drug due to its potent stimulant and euphoric effects and is considered to be addictive, with both physical and psychological withdrawal occurring if its use is discontinued after prolonged or high-dosage administration. It is usually snorted, but can be smoked, injected, or taken orally.

<span class="mw-page-title-main">Phenethylamine</span> Organic compound, a stimulant in humans

Phenethylamine (PEA) is an organic compound, natural monoamine alkaloid, and trace amine, which acts as a central nervous system stimulant in humans. In the brain, phenethylamine regulates monoamine neurotransmission by binding to trace amine-associated receptor 1 (TAAR1) and inhibiting vesicular monoamine transporter 2 (VMAT2) in monoamine neurons. To a lesser extent, it also acts as a neurotransmitter in the human central nervous system. In mammals, phenethylamine is produced from the amino acid L-phenylalanine by the enzyme aromatic L-amino acid decarboxylase via enzymatic decarboxylation. In addition to its presence in mammals, phenethylamine is found in many other organisms and foods, such as chocolate, especially after microbial fermentation.

<span class="mw-page-title-main">Monoamine transporter</span> Proteins that function as integral plasma-membrane transporters

Monoamine transporters (MATs) are proteins that function as integral plasma-membrane transporters to regulate concentrations of extracellular monoamine neurotransmitters. The three major classes are serotonin transporters (SERTs), dopamine transporters (DATs), and norepinephrine transporters (NETs) and are responsible for the reuptake of their associated amine neurotransmitters. MATs are located just outside the synaptic cleft (peri-synaptically), transporting monoamine transmitter overflow from the synaptic cleft back to the cytoplasm of the pre-synaptic neuron. MAT regulation generally occurs through protein phosphorylation and post-translational modification. Due to their significance in neuronal signaling, MATs are commonly associated with drugs used to treat mental disorders as well as recreational drugs. Compounds targeting MATs range from medications such as the wide variety of tricyclic antidepressants, selective serotonin reuptake inhibitors such as fluoxetine (Prozac) to stimulant medications such as methylphenidate (Ritalin) and amphetamine in its many forms and derivatives methamphetamine (Desoxyn) and lisdexamfetamine (Vyvanse). Furthermore, drugs such as MDMA and natural alkaloids such as cocaine exert their effects in part by their interaction with MATs, by blocking the transporters from mopping up dopamine, serotonin, and other neurotransmitters from the synapse.

<span class="mw-page-title-main">Dextroamphetamine</span> CNS stimulant and isomer of amphetamine

Dextroamphetamine (INN:dexamfetamine) is a potent central nervous system (CNS) stimulant and enantiomer of amphetamine that is prescribed for the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy. It is also used as an athletic performance and cognitive enhancer, and recreationally as an aphrodisiac and euphoriant.

Stimulant psychosis is a mental disorder characterized by psychotic symptoms. It involves and typically occurs following an overdose or several day binge on psychostimulants; however, one study reported occurrences at regularly prescribed doses in approximately 0.1% of individuals within the first several weeks after starting amphetamine or methylphenidate therapy. Methamphetamine psychosis, or long-term effects of stimulant use in the brain, depend upon genetics and may persist for some time.

<span class="mw-page-title-main">Adderall</span> Drug mixture used mainly to treat ADHD and narcolepsy

Adderall and Mydayis are trade names for a combination drug called mixed amphetamine salts containing four salts of amphetamine. The mixture is composed of equal parts racemic amphetamine and dextroamphetamine, which produces a (3:1) ratio between dextroamphetamine and levoamphetamine, the two enantiomers of amphetamine. Both enantiomers are stimulants, but differ enough to give Adderall an effects profile distinct from those of racemic amphetamine or dextroamphetamine, which are marketed as Evekeo and Dexedrine/Zenzedi, respectively. Adderall is used in the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy. It is also used illicitly as an athletic performance enhancer, cognitive enhancer, appetite suppressant, and recreationally as a euphoriant. It is a central nervous system (CNS) stimulant of the phenethylamine class.

A dopamine reuptake inhibitor (DRI) is a class of drug which acts as a reuptake inhibitor of the monoamine neurotransmitter dopamine by blocking the action of the dopamine transporter (DAT). Reuptake inhibition is achieved when extracellular dopamine not absorbed by the postsynaptic neuron is blocked from re-entering the presynaptic neuron. This results in increased extracellular concentrations of dopamine and increase in dopaminergic neurotransmission.

<span class="mw-page-title-main">Pemoline</span> Stimulant, used in the treatment of ADHD

Pemoline, sold under the brand name Cylert among others, is a stimulant medication which has been used in the treatment of attention-deficit hyperactivity disorder (ADHD) and narcolepsy. It has been discontinued in most countries due to rare but serious problems with liver toxicity. The medication was taken by mouth.

Cross-tolerance is a phenomenon that occurs when tolerance to the effects of a certain drug produces tolerance to another drug. It often happens between two drugs with similar functions or effects—for example, acting on the same cell receptor or affecting the transmission of certain neurotransmitters. Cross-tolerance has been observed with pharmaceutical drugs such as anti-anxiety agents and illicit substances, and sometimes the two of them together. Often, a person who uses one drug can be tolerant to a drug that has a completely different function. This phenomenon allows one to become tolerant to a drug that they have never used before.

<span class="mw-page-title-main">Dopaminergic</span> Substance related to dopamine functions

Dopaminergic means "related to dopamine" (literally, "working on dopamine"), dopamine being a common neurotransmitter. Dopaminergic substances or actions increase dopamine-related activity in the brain. Dopaminergic brain pathways facilitate dopamine-related activity. For example, certain proteins such as the dopamine transporter (DAT), vesicular monoamine transporter 2 (VMAT2), and dopamine receptors can be classified as dopaminergic, and neurons that synthesize or contain dopamine and synapses with dopamine receptors in them may also be labeled as dopaminergic. Enzymes that regulate the biosynthesis or metabolism of dopamine such as aromatic L-amino acid decarboxylase or DOPA decarboxylase, monoamine oxidase (MAO), and catechol O-methyl transferase (COMT) may be referred to as dopaminergic as well. Also, any endogenous or exogenous chemical substance that acts to affect dopamine receptors or dopamine release through indirect actions (for example, on neurons that synapse onto neurons that release dopamine or express dopamine receptors) can also be said to have dopaminergic effects, two prominent examples being opioids, which enhance dopamine release indirectly in the reward pathways, and some substituted amphetamines, which enhance dopamine release directly by binding to and inhibiting VMAT2.

<span class="mw-page-title-main">Lisdexamfetamine</span> Central nervous system stimulant prodrug

Lisdexamfetamine, sold under the brand names Vyvanse and Elvanse among others, is a stimulant medication that is used to treat attention deficit hyperactivity disorder (ADHD) in children and adults and for moderate-to-severe binge eating disorder in adults. Lisdexamfetamine is taken by mouth. Its effects generally begin within two hours and last for up to 14 hours. In the United Kingdom, it is usually less preferred to methylphenidate for the treatment of children.

<span class="mw-page-title-main">Methamphetamine</span> Central nervous system stimulant

Methamphetamine is a potent central nervous system (CNS) stimulant that is mainly used as a recreational drug and less commonly as a second-line treatment for attention deficit hyperactivity disorder and obesity. Methamphetamine was discovered in 1893 and exists as two enantiomers: levo-methamphetamine and dextro-methamphetamine. Methamphetamine properly refers to a specific chemical substance, the racemic free base, which is an equal mixture of levomethamphetamine and dextromethamphetamine in their pure amine forms, but the hydrochloride salt, commonly called crystal meth, is widely used. Methamphetamine is rarely prescribed over concerns involving human neurotoxicity and potential for recreational use as an aphrodisiac and euphoriant, among other concerns, as well as the availability of safer substitute drugs with comparable treatment efficacy such as Adderall and Vyvanse. Dextromethamphetamine is a stronger CNS stimulant than levomethamphetamine.

<span class="mw-page-title-main">Monoamine releasing agent</span> Class of compounds

A monoamine releasing agent (MRA), or simply monoamine releaser, is a drug that induces the release of a monoamine neurotransmitter from the presynaptic neuron into the synapse, leading to an increase in the extracellular concentrations of the neurotransmitter. Many drugs induce their effects in the body and/or brain via the release of monoamine neurotransmitters, e.g., trace amines, many substituted amphetamines, and related compounds.

<span class="mw-page-title-main">Norepinephrine releasing agent</span> Catecholaminergic type of drug

A norepinephrine releasing agent (NRA), also known as an adrenergic releasing agent, is a catecholaminergic type of drug that induces the release of norepinephrine (noradrenaline) and epinephrine (adrenaline) from the pre-synaptic neuron into the synapse. This in turn leads to increased extracellular concentrations of norepinephrine and epinephrine therefore an increase in adrenergic neurotransmission.

Substituted amphetamines are a class of compounds based upon the amphetamine structure; it includes all derivative compounds which are formed by replacing, or substituting, one or more hydrogen atoms in the amphetamine core structure with substituents. The compounds in this class span a variety of pharmacological subclasses, including stimulants, empathogens, and hallucinogens, among others. Examples of substituted amphetamines are amphetamine (itself), methamphetamine, ephedrine, cathinone, phentermine, mephentermine, tranylcypromine, bupropion, methoxyphenamine, selegiline, amfepramone (diethylpropion), pyrovalerone, MDMA (ecstasy), and DOM (STP).

A monoamine reuptake inhibitor (MRI) is a drug that acts as a reuptake inhibitor of one or more of the three major monoamine neurotransmitters serotonin, norepinephrine, and dopamine by blocking the action of one or more of the respective monoamine transporters (MATs), which include the serotonin transporter (SERT), norepinephrine transporter (NET), and dopamine transporter (DAT). This in turn results in an increase in the synaptic concentrations of one or more of these neurotransmitters and therefore an increase in monoaminergic neurotransmission.

References

  1. 1 2 3 4 5 Cao DN, Shi JJ, Hao W, Wu N, Li J (June 2016). "Advances and challenges in pharmacotherapeutics for amphetamine-type stimulants addiction". European Journal of Pharmacology. 780: 129–35. doi:10.1016/j.ejphar.2016.03.040. PMID   27018393.
  2. 1 2 3 McCreary AC, Mueller CP, Filip M (January 2015). "Psychostimulants: basic and clinical pharmacology.". In Taba P, Lees A, Sikk K (eds.). International Review of Neurobiology. The Neuropsychiatric Complications of Stimulant Abuse. Vol. 120. Academic Press. pp. 41–83. doi:10.1016/bs.irn.2015.02.008. ISBN   9780128029787. PMID   26070753.
  3. Edeleano L (1887). "Ueber einige Derivate der Phenylmethacrylsäure und der Phenylisobuttersäure". Berichte der Deutschen Chemischen Gesellschaft. 20 (1): 616–622. doi:10.1002/cber.188702001142. ISSN   1099-0682.
  4. 1 2 Terminology and Information on Drugs: Third Edition. United Nations. 2016. doi:10.18356/0f5bdc21-en. ISBN   9789210579148 . Retrieved 2020-03-29.{{cite book}}: |website= ignored (help)
  5. 1 2 3 4 5 6 Rasmussen N (January 2015). "Amphetamine-Type Stimulants: The Early History of Their Medical and Non-Medical Uses". In Taba P, Lees A, Sikk K (eds.). International Review of Neurobiology. The Neuropsychiatric Complications of Stimulant Abuse. Vol. 120. Academic Press. pp. 9–25. doi:10.1016/bs.irn.2015.02.001. ISBN   9780128029787. PMID   26070751.
  6. 1 2 "Ectasy: MDMA and other ring-substituted amphetamines". World Health Organization.
  7. Mitchell CM, El Jordi O, Yamamoto BK (January 2019). "Inflammatory mechanisms of abused drugs.". In Aschner M, Costa LG (eds.). Advances in Neurotoxicology. Role of Inflammation in Environmental Neurotoxicity. Vol. 3. Academic Press. pp. 133–168. doi:10.1016/bs.ant.2018.10.006. ISBN   9780128157176. S2CID   87635740.
  8. Maurice T, Su TP (November 2009). "The pharmacology of sigma-1 receptors". Pharmacology & Therapeutics. 124 (2): 195–206. doi:10.1016/j.pharmthera.2009.07.001. PMC   2785038 . PMID   19619582.
  9. 1 2 Jiao D, Liu Y, Li X, Liu J, Zhao M (2015). "The role of the GABA system in amphetamine-type stimulant use disorders". Frontiers in Cellular Neuroscience. 9: 162. doi: 10.3389/fncel.2015.00162 . PMC   4419710 . PMID   25999814.
  10. 1 2 Ito K, Ohmori T, Abekawa T, Koyama T (April 2000). "The role of benzodiazepine receptors in the acquisition and expression of behavioral sensitization to methamphetamine". Pharmacology, Biochemistry, and Behavior. 65 (4): 705–10. doi:10.1016/s0091-3057(99)00263-4. PMID   10764926. S2CID   22812444.
  11. Fischer A (2013). Link between amphetamine-type stimulant use and the transmission of HIV and other blood-borne viruses in the Southeast Asia region. Australian National Council on Drugs. ISBN   978-87-7018-279-9. OCLC   814364399.
  12. 1 2 Cruickshank CC, Dyer KR (July 2009). "A review of the clinical pharmacology of methamphetamine". Addiction. 104 (7): 1085–99. doi: 10.1111/j.1360-0443.2009.02564.x . PMID   19426289. S2CID   37079117.
  13. 1 2 3 "Department of Health | Pharmacology of amphetamines". www1.health.gov.au. Retrieved 2020-03-29.
  14. 1 2 3 "Amphetamine (PIM 934)". www.inchem.org. Retrieved 2020-03-29.
  15. "Methylphenidate". www.drugbank.ca. Retrieved 2020-03-29.
  16. "Canadian ADHD Practice Guidelines (CAP-Guidelines)" (PDF). Canadian ADHD Resource Alliance.
  17. "Medications". Center for Narcolepsy. Retrieved 2020-03-29.
  18. Mignot EJ (October 2012). "A practical guide to the therapy of narcolepsy and hypersomnia syndromes". Neurotherapeutics. 9 (4): 739–52. doi:10.1007/s13311-012-0150-9. PMC   3480574 . PMID   23065655.
  19. "Narcolepsy Fact Sheet | National Institute of Neurological Disorders and Stroke". www.ninds.nih.gov. Retrieved 2020-03-29.
  20. Center for Substance Abuse Treatment (2005). Appendix C: Glossary of Terms. Substance Abuse and Mental Health Services Administration (US).
  21. 1 2 3 4 "WHO Multi-Site Project on Methamphetamine-Induced Psychosis: A descriptive report of findings from participating countries" (PDF). WHO.
  22. "World Drug Report 2013" (PDF). United Nations Office on Drugs and Crime.
  23. 1 2 Madea B (2014-03-14). "History of Forensic Medicine". Handbook of Forensic Medicine. John Wiley & Sons, Ltd. pp. 1–14. doi:10.1002/9781118570654.ch1. ISBN   978-1-118-57065-4.
  24. 1 2 Richards JR, Albertson TE, Derlet RW, Lange RA, Olson KR, Horowitz BZ (May 2015). "Treatment of toxicity from amphetamines, related derivatives, and analogues: a systematic clinical review". Drug and Alcohol Dependence. 150: 1–13. doi:10.1016/j.drugalcdep.2015.01.040. PMID   25724076.
  25. Connell PH (August 1954). "SUCCESSFUL regional Whitley appeal: up-grading of S.H.M.O. post". British Medical Journal. 2 (Suppl 2588): 101–2. PMC   1974659 . PMID   13182277.
  26. "Amphetamine drug profile | www.emcdda.europa.eu". www.emcdda.europa.eu. Retrieved 2020-03-29.
  27. Curran C, Byrappa N, McBride A (September 2004). "Stimulant psychosis: systematic review". The British Journal of Psychiatry. 185 (3): 196–204. doi: 10.1192/bjp.185.3.196 . PMID   15339823.
  28. Magor-Blatch, Lynne (2013). Intervention for Amphetamine-type Stimulant Use in the Therapeutic Community (Thesis). UNSW Sydney. doi:10.26190/unsworks/16215. hdl:1959.4/52737.
  29. Tran M, Luong Q, Le G, Dunne M, Baker P (June 2021). "Psychosocial Interventions for Amphetamine Type Stimulant Use Disorder: An Overview of Systematic Reviews". Frontiers in Psychiatry. 12 (834): 196–204. doi: 10.3389/fpsyt.2021.512076 . PMC   8245759 . PMID   34220557.