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Monoamine releasing agent

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"Releasing agent" redirects here. For mold release agents, see Release agent.

Amphetamine, the prototypical monoamine releasing agent, which acts on norepinephrine and dopamine.

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.

Types of MRAs

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MRAs can be classified by the monoamines they mainly release, although these drugs lie on a spectrum.

MRAs must be distinguished from monoamine reuptake inhibitors and monoaminergic activity enhancers, which work via distinct mechanisms.

Endogenous MRAs

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A number of endogenous compounds are known to act as MRAs.[1][2][3][4][5] These include the monoamine neurotransmitters dopamine (an NDRA),[2] norepinephrine (an NDRA),[2] and serotonin (an SRA) themselves,[2] as well as the trace amines phenethylamine (an NDRA),[5][6][7][8] tryptamine (an SDRA or imbalanced SNDRA),[3][4] and tyramine (an NDRA).[2][1] Synthetic MRAs are substantially based on structural modification of these endogenous compounds, most prominently including the substituted phenethylamines and substituted tryptamines.[2][9][10][3][11][12][13] Release of monoamine neurotransmitters by themselves, for instance in the cases of serotonin, norepinephrine, and dopamine, has been referred to as "self-release".[1] The physiological significance of the findings that monoamine neurotransmitters can act as releasing agents of themselves is unclear.[1] However, it could imply that efflux is a common neurotransmitter regulatory mechanism that can be induced by any transporter substrate.[1] It is possible that it could be a protective mechanism of some sort.[1]

Mechanism of action

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Main article: Amphetamine § Pharmacodynamics

MRAs cause the release of monoamine neurotransmitters by various complex mechanisms of action. They may enter the presynaptic neuron primarily via plasma membrane transporters, such as the dopamine transporter (DAT), norepinephrine transporter (NET), and serotonin transporter (SERT). Some, such as exogenous phenethylamine, amphetamine, and methamphetamine, can also diffuse directly across the cell membrane to varying degrees. Once inside the presynaptic neuron, they may inhibit the reuptake of monoamine neurotransmitters through vesicular monoamine transporter 2 (VMAT2) and release the neurotransmitters stores of synaptic vesicles into the cytoplasm by inducing reverse transport at VMAT2. MRAs can also bind to the intracellular receptor TAAR1 as agonists, which triggers a phosphorylation cascade via protein kinases that results in the phosphorylation of monoamine transporters located at the plasma membrane (i.e., the dopamine transporter, norepinephrine transporter, and serotonin transporter); upon phosphorylation, these transporters transport monoamines in reverse (i.e., they move monoamines from the neuronal cytoplasm into the synaptic cleft).[14] The combined effects of MRAs at VMAT2 and TAAR1 result in the release of neurotransmitters out of synaptic vesicles and the cell cytoplasm into the synaptic cleft where they bind to their associated presynaptic autoreceptors and postsynaptic receptors. Certain MRAs interact with other presynaptic intracellular receptors which promote monoamine neurotransmission as well (e.g., methamphetamine is also an agonist at σ1 receptor).

In spite of findings that TAAR1 activation by amphetamines can reverse the monoamine transporters and mediate monoamine release however,[14][15][16][17] major literature reviews on monoamine releasing agents by experts like Richard B. Rothman and David J. Heal state that the nature of monoamine transport reversal is not well understood and/or do not mention TAAR1 activation.[18][19][20][21] Moreover, amphetamines continue to produce psychostimulant-like effects and induction of dopamine and norepinephrine release in TAAR1 knockout mice.[14][22][23][24][25] In fact, TAAR1 knockout mice are supersensitive to the effects of amphetamines and TAAR1 activation appears to inhibit the striatal dopaminergic effects of psychostimulants.[14][23][22][24][25] Additionally, many substrate-type MRAs that do not bind to and/or activate the (human) TAAR1 are known, including most cathinones, ephedrine, 4-methylamphetamine, and 4-methylaminorex derivatives, among others.[26][27][28][29]

There is a constrained and relatively small molecular size requirement for compounds to act as monoamine releasing agents.[18] This is because they must be small enough to serve as substrates of the monoamine transporters and thereby be transported inside of monoaminergic neurons by these proteins, in turn allowing them to induce monoamine neurotransmitter release.[18] Compounds with chemical features extending beyond the size constraints for releasers will instead act as partial releasers, reuptake inhibitors, or be inactive.[18] Partial releasers show reduced maximal efficacy in releasing monoamine neurotransmitters compared to conventional full releasers.[18]

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Dopamine reuptake inhibitors (DRIs) have been grouped into two types, typical or conventional DRIs like cocaine, WIN-35428 (β-CFT), and methylphenidate that produce potent psychostimulant, euphoric, and reinforcing effects, and atypical DRIs like vanoxerine (GBR-12909), modafinil, benztropine, and bupropion, which do not produce such effects or have greatly reduced such effects.[21][19][5][30] It has been proposed that typical DRIs may not actually be acting primarily as DRIs but rather as dopamine releasing agents (DRAs) via mechanisms distinct from conventional substrate-type DRAs like amphetamines.[21] A variety of different pieces of evidence support this hypothesis and help to explain otherwise confusing findings.[21] Under this model, typical cocaine-like DRIs have been referred to with the new label of dopamine transporter (DAT) "inverse agonists" to distinguish them from conventional substrate-type DRAs.[21] An alternative theory is that typical DRIs and atypical DRIs stabilize the DAT in different conformations, with typical DRIs resulting in an outward-facing open conformation that produces differing pharmacological effects from those of atypical DRIs.[19][5][30][31]

Some MRAs, like the amphetamines amphetamine and methamphetamine, as well as trace amines like phenethylamine, tryptamine, and tyramine, are additionally monoaminergic activity enhancers (MAEs).[32][33][6] That is, they induce the action potential-mediated release of monoamine neurotransmitters (in contrast to MRAs, which induced uncontrolled monoamine release independent of neuronal firing).[32][33][6] They are usually active as MAEs at much lower concentrations than those at which they induce monoamine release.[32][33][6] The MAE actions of MAEs may be mediated by TAAR1 agonism, which has likewise been implicated in monoamine-releasing actions.[34][35] MAEs without concomitant potent monoamine-releasing actions, like selegiline (L-deprenyl), phenylpropylaminopentane (PPAP), and benzofuranylpropylaminopentane (BPAP), have been developed.[32][33]

Effects and uses

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MRAs can have a wide variety of effects depending upon their selectivity for inducing release of different monoamine neurotransmitters.

Selective SRAs such as fenfluramine and related compounds are described as dysphoric and lethargic in lower doses, and in higher doses some hallucinogenic effects have been reported.[36][37] Less selective SRAs that also stimulate the release of dopamine, such as methylenedioxymethamphetamine (MDMA), are described as more pleasant, elevating mood and increasing energy and sociability.[38] SRAs have been used as appetite suppressants and as entactogens. They have also been proposed for use as more effective antidepressants and anxiolytics than selective serotonin reuptake inhibitors (SSRIs) because they can produce much larger increases in serotonin levels in comparison.[39]

DRAs, usually non-selective for both norepinephrine and dopamine, have psychostimulant effects, causing an increase in energy, motivation, elevated mood, and euphoria.[40] Other variables can significantly affect the subjective effects, such as infusion rate (increasing positive effects of DRAs) and psychological expectancy effects.[41] They are used in the treatment of attention deficit hyperactivity disorder (ADHD), as appetite suppressants, wakefulness-promoting agents, to improve motivation, and are drugs of recreational use and misuse.

Selective NRAs are minimally psychoactive, but as demonstrated by ephedrine, may be distinguished from placebo, and may trends towards liking.[42] They may also be performance-enhancing,[43] in contrast to reboxetine which is solely a norepinephrine reuptake inhibitor.[44][45] In addition to their central effects, NRAs produce peripheral sympathomimetic effects like increased heart rate, blood pressure, and force of heart contractions. They are used as nasal decongestants and bronchodilators, but have also seen use as wakefulness-promoting agents, appetite suppressants, and antihypotensive agents. They have additionally seen use as performance-enhancing drugs, for instance in sports.

Selectivity

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MRAs act to varying extents on serotonin, norepinephrine, and dopamine. Some induce the release of all three neurotransmitters to a similar degree, like methylenedioxymethamphetamine (MDMA), while others are more selective. As examples, amphetamine and methamphetamine are NDRAs but only very weak releasers of serotonin (~60- and 30-fold less than of dopamine, respectively) and MBDB is a fairly balanced SNRA but a weak releaser of dopamine (~6- and 10-fold lower of dopamine than of norepinephrine or serotonin, respectively). Even more selective include agents like fenfluramine, a selective SRA, and ephedrine, a selective NRA. The differences in selectivity of these agents is the result of different affinities as substrates for the monoamine transporters, and thus differing ability to gain access into monoaminergic neurons and induce monoamine neurotransmitter release via the TAAR1 and VMAT2 proteins.

As of present, no selective DRAs are known. This is because it has proven extremely difficult to separate DAT affinity from NET affinity and retain releasing efficacy at the same time.[46] Several selective SDRAs, including tryptamine, (+)-α-ethyltryptamine (αET), 5-chloro-αMT, and 5-fluoro-αET, are known.[4][47] However, besides their serotonin release, these compounds additionally act as non-selective serotonin receptor agonists, including of the serotonin 5-HT2A receptor (with accompanying hallucinogenic effects), and some of them are known to act as monoamine oxidase inhibitors.[4][47]

Neurotoxicity

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Some MRAs have been found to act as monoaminergic neurotoxins and hence to produce long-lasting damage to monoaminergic neurons.[48][49] Examples include dopaminergic neurotoxicity with amphetamine and methamphetamine and serotonergic neurotoxicity with methylenedioxymethamphetamine (MDMA).[48][49] Amphetamine may produce significant dopaminergic neurotoxicity even at therapeutic doses.[50][51][52][53][54][55] However, clinical doses of amphetamine producing neurotoxicity is controversial and disputed.[56][50][52] In contrast to amphetamines, monoamine reuptake inhibitors like methylphenidate lack apparent neurotoxic effects.[50]

Analogues of MDMA with retained MRA activity but reduced or no serotonergic neurotoxicity, like 5,6-methylenedioxy-2-aminoindane (MDAI) and 5-iodo-2-aminoindane (5-IAI), have been developed.[57][58] Certain drugs have been found to block the neurotoxicity of MRAs in animals.[49] For instance, the selective MAO-B inhibitor selegiline has been found to prevent the serotonergic neurotoxicity of MDMA in rodents.[49]

Activity profiles

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See also: Monoamine reuptake inhibitor § Binding profiles
Activity profiles of MRAs (EC50, nM)[9][10]
Compound 5-HTTooltip Serotonin NETooltip Norepinephrine DATooltip Dopamine Type Class Ref
2-Aminoindane >10000 86 439 NDRA Aminoindane [59]
2C-E >100000 >100000 >100000 IA Phenethylamine [60]
2C-I >100000 >100000 >100000 IA Phenethylamine [60]
3-Chloroamphetamine ND 9.4 11.8 ND Amphetamine [61][1]
3-Chloromethcathinone 211 19 26 SNDRA Cathinone [5]
3-Fluoroamphetamine 1937 16.1 24.2 NDRA Amphetamine [62][1]
3-Methoxyamphetamine ND 58.0 103 ND Amphetamine [1]
3-Methoxy-4-hydroxyamphetamine (HMA) ND 694 1450 ND Amphetamine [1]
3-Methoxy-4-hydroxymethamphetamine (HMMA) ND 625 607 ND Amphetamine [1]
3-Methoxymethcathinone 306 ND (68% at 10 μM) 129 SDRA Cathinone [63]
3-Methylamphetamine 218 18.3 33.3 NDRA Amphetamine [62][61][1]
3-Methylmethcathinone 292 27 70 SNDRA Cathinone [5]
3,4-Dihydroxyamphetamine (HHA; α-methyl-DA) ND 33 3485 ND Amphetamine [1]
3,4-Dihydroxymethamphetamine (HHMA; N-Me-α-Me-DA) ND 77 1729 ND Amphetamine [1]
4-Chloroamphetamine ND 23.5 68.5 SNDRA Amphetamine [61][1]
4-Fluoroamphetamine 730–939 28.0–37 51.5–200 NDRA Amphetamine [62][60][61][1]
4-Methoxyamphetamine ND 166 867 ND Amphetamine [1]
cis-4-Methylaminorex 53.2 4.8 1.7 NDRA Aminorex [64]
4-Methylamphetamine 53.4 22.2 44.1 SNDRA Amphetamine [62][61][1]
4-Methylphenethylamine ND ND 271 ND Phenethylamine [5]
4-Methylthiomethamphetamine 21 ND ND ND Amphetamine [65]
4,4'-Dimethylaminorex ND ND ND SNDRA Aminorex ND
  cis-4,4'-Dimethylaminorex 17.7–18.5 11.8–26.9 8.6–10.9 SNDRA Aminorex [64][66]
  trans-4,4'-Dimethylaminorex 59.9 31.6 24.4 SNDRA Aminorex [66]
5-(2-Aminopropyl)indole (5-IT) 28–104.8 13.3–79 12.9–173 SNDRA Amphetamine [47][67]
  (R)-5-(2-Aminopropyl)indole 177 81 1062 SNRA Amphetamine [47]
  (S)-5-(2-Aminopropyl)indole ND ND ND SNDRA Amphetamine ND
5-Chloro-αMT 16 3434 54 SDRA Tryptamine [4][47]
5-Fluoro-αET 36.6 5334 150 SDRA Tryptamine [4]
5-Fluoro-αMT 19 126 32 SNDRA Tryptamine [47]
5-MeO-αMT 460 8900 1500 SNDRA Tryptamine [60]
5-MeO-AI 134 861 2646 SNRA Aminoindane [59]
5-MeO-DMT >100000 >100000 >100000 IA Tryptamine [60]
6-(2-Aminopropyl)indole (6-IT) 19.9 25.6 164.0 SNDRA Amphetamine [67]
6-Chloroamphetamine ND 19.1 62.4 ND Amphetamine [1]
6-Fluoroamphetamine ND 24.1 38.1 ND Amphetamine [1]
6-Methoxyamphetamine ND 473 1478 ND Amphetamine [1]
6-Methylamphetamine ND 37 127 ND Amphetamine [1]
α-Ethyltryptamine 23.2 640 232 SDRA Tryptamine [4]
α-Methyltryptamine 21.7–68 79–112 78.6–180 SNDRA Tryptamine [60][4]
Amfepramone (diethylpropion) >10000 >10000 >10000 PD Cathinone [68]
Aminorex 193–414 15.1–26.4 9.1–49.4 SNDRA Aminorex [2][64][1]
Amphetamine ND ND ND NDRA Amphetamine ND
  D-Amphetamine 698–1765 6.6–10.2 5.8–24.8 NDRA Amphetamine [2][69][1]
  L-Amphetamine ND 9.5 27.7 NDRA Amphetamine [61][1]
β-Ketophenethylamine (phenacylamine) >10000 ND 208 ND Phenethylamine [5][63]
BDB 180 540 2,300 NDRA Amphetamine [60]
Benzylpiperazine ≥6050 62–68 175–600 NDRA Arylpiperazine [60][70][10][1]
Bufotenin 30.5 >10000 >10000 SRA Tryptamine [3]
Butylamphetamine ND ND IA ND Amphetamine [5]
Cathinone 6100 23.6 83.1 NDRA Cathinone [1][63]
  D-Cathinone ND ND ND NRA Cathinone ND
  L-Cathinone 2366 12.4 18.5 NDRA Cathinone [71]
Chlorphentermine 30.9 >10000 2650 SRA Amphetamine [2]
DMPP 26 56 1207 SNRA Arylpiperazine [65]
DMT 114 4166 >10000 SRA Tryptamine [3]
Dopamine >10000 (RI) 66.2 86.9 NDRA Phenethylamine [2][1]
DPT >100000 >100000 >100000 IA Tryptamine [60][3]
Ephedrine (racephedrine) ND ND ND NDRA Cathinol ND
  D-Ephedrine (ephedrine) >10000 43.1–72.4 236–1350 NDRA Cathinol [2][1]
  L-Ephedrine >10000 218 2104 NRA Cathinol [2][71]
Epinephrine ND ND ND NDRA Phenethylamine ND
Ethcathinone 2118 99.3 >1000 (RI) NRA Cathinone [68][1]
Ethylamphetamine ND ND 296 ND Amphetamine [5]
Fenfluramine 79.3–108 739 >10000 (RI) SRA Amphetamine [2][72][73][1]
  D-Fenfluramine 51.7 302 >10000 SNRA Amphetamine [2][72]
  L-Fenfluramine 147 >10000 >10000 SRA Amphetamine [72][74]
MBDB 540 3300 >100000 SNRA Amphetamine [60]
mCPP 28–38.1 ≥1400 63000 SRA Arylpiperazine [60][74][75]
MDA 160 108 190 SNDRA Amphetamine [73][1]
  (R)-MDA 310 290 900 SNDRA Amphetamine [73][1]
  (S)-MDA 100 50.0 98.5 SNDRA Amphetamine [73][1]
MDAI 114 117 1334 SNRA Aminoindane [59]
MDEA 47 2608 622 SNDRA Amphetamine [65]
  (R)-MDEA 52 651 507 SNDRA Amphetamine [65]
  (S)-MDEA 465 RI RI SRA Amphetamine [65]
MDMA 49.6–72 54.1–110 51.2–278 SNDRA Amphetamine [2][76][67][73][1]
  (R)-MDMA 340 560 3700 SNDRA Amphetamine [73][1]
  (S)-MDMA 74 136 142 SNDRA Amphetamine [73][1]
MDMAR ND ND ND SNDRA Aminorex ND
  cis-MDMAR 43.9 14.8 10.2 SNDRA Aminorex [66]
  trans-MDMAR 73.4 38.9 36.2 SNDRA Aminorex [66]
Mephedrone 118.3–122 58–62.7 49.1–51 SNDRA Cathinone [76][69]
Methamnetamine 13 34 10 SNDRA Amphetamine [65]
Methamphetamine ND ND ND NDRA Amphetamine ND
  D-Methamphetamine 736–1291.7 12.3–13.8 8.5–24.5 NDRA Amphetamine [2][76][1]
  L-Methamphetamine 4640 28.5 416 NRA Amphetamine [2][1]
Methcathinone ND 22.4 49.9 NDRA Cathinone [1]
  D-Methcathinone ND ND ND NRA Cathinone ND
  L-Methcathinone 1772 13.1 14.8 NDRA Cathinone [71]
Methylone 234–242.1 140–152.3 117–133.0 SNDRA Cathinone [76][69]
MMAI 31 3101 >10000 SRA Aminoindane [59]
Naphthylisopropylamine 3.4 11.1 12.6 SNDRA Amphetamine [77][1]
Norephedrine (phenylpropanolamine) ND ND ND NDRA Cathinol ND
  D-Norephedrine >10000 42.1 302 NDRA Cathinol [71]
  L-Norephedrine >10000 137 1371 NRA Cathinol [71]
Norepinephrine >10000 164 869 NDRA Phenethylamine [2][1]
Norfenfluramine 104 168–170 1900–1925 SNRA Amphetamine [72][73]
  (+)-Norfenfluramine 59.3 72.7 924 SNRA Amphetamine [72]
  (–)-Norfenfluramine 287 474 >10000 SNRA Amphetamine [72]
Norpropylhexedrine ND ND ND NDRA Cyclohexethylamine ND
Norpseudoephedrine ND ND ND NDRA Cathinol ND
  D-Norpseudoephedrine (cathine) >10000 15.0 68.3 NDRA Cathinol [71]
  L-Norpseudoephedrine >10000 30.1 294 NDRA Cathinol [71]
oMPP 175 39.1 296–542 SNDRA Arylpiperazine [78][5]
PAL-738 23 65 58 SNDRA Phenylmorpholine [65]
PAL-874 >10000 305 688 NDRA Phenylbutynamine [65]
Phendimetrazine >100000 >10000 >10000 PD Phenylmorpholine [79][1]
Phenethylamine >10000 10.9 39.5 NDRA Phenethylamine [5][61][1]
Phenmetrazine 7765 50.4 131 NDRA Phenylmorpholine [79][1]
Phentermine 3511 39.4 262 NDRA Amphetamine [2][1]
Phenylalaninol ND ND ND ND Amphetamine ND
  D-Phenylalaninol >10000 106 1355 NRA Amphetamine [78]
  L-Phenylalaninol ND ND ND ND Amphetamine ND
Phenylisobutylamine ND ND 225 ND Amphetamine [5]
Phenylpropylamine ND 222 1491 NDRA Phenylpropylamine [61][1]
pMPP 3200 1500 11000 SNRA Arylpiperazine [60]
pNPP 43 >10000 >10000 SRA Arylpiperazine [65]
Propylamphetamine ND ND RI (1013) ND Amphetamine [5]
Propylhexedrine ND ND ND NDRA Cyclohexethylamine ND
Pseudoephedrine (racemic pseudoephedrine) ND ND ND NDRA Cathinol ND
  D-Pseudoephedrine >10000 4092 9125 NDRA Cathinol [71]
  L-Pseudoephedrine (pseudoephedrine) >10000 224 1988 NRA Cathinol [71]
Pseudophenmetrazine >10000 514 RI NRA Phenylmorpholine [79]
Psilocin 561 >10000 >10000 SRA Tryptamine [65][3]
Serotonin 44.4 >10000 (RI) ≥1960 SRA Tryptamine [2][1]
TFMCPP 33 >10000 >10000 SRA Arylpiperazine [65]
TFMPP 121 >10000 >10000 SRA Arylpiperazine [70][1]
Trimethoxyamphetamine 16000 >100000 >100000 IA Amphetamine [60]
Tryptamine 32.6 716 164 SDRA Tryptamine [3][4]
Tyramine 2775 40.6 119 NDRA Phenethylamine [2][1]
Notes: The smaller the value, the more strongly the substance releases the neurotransmitter.

See also

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References

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  1. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax Blough B (July 2008). "Dopamine-releasing agents". Dopamine Transporters: Chemistry, Biology and Pharmacology. Hoboken [NJ]: Wiley. pp. 305–320. ISBN 978-0-470-11790-3. Archived from the original on 3 November 2024. TABLE 11-2 Comparison of the DAT- and NET-Releasing Activity of a Series of Amphetamines [...]
  2. ^ a b c d e f g h i j k l m n o p q r s t u Rothman RB, Baumann MH, Dersch CM, Romero DV, Rice KC, Carroll FI, et al. (January 2001). "Amphetamine-type central nervous system stimulants release norepinephrine more potently than they release dopamine and serotonin". Synapse. 39 (1): 32–41. doi:10.1002/1098-2396(20010101)39:1<32::AID-SYN5>3.0.CO;2-3. PMID 11071707. S2CID 15573624.
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  13. ^ Shulgin A, Manning T, Daley PF (2011). The Shulgin Index: Psychedelic Phenethylamines and Related Compounds. Vol. 1. Transform Press. ISBN 978-0-9630096-3-0. Retrieved 2024-08-18.
  14. ^ a b c d Miller GM (January 2011). "The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity". Journal of Neurochemistry. 116 (2): 164–176. doi:10.1111/j.1471-4159.2010.07109.x. PMC 3005101. PMID 21073468.
  15. ^ Wu R, Liu J, Li JX (2022). "Trace amine-associated receptor 1 and drug abuse". Behavioral Pharmacology of Drug Abuse: Current Status. Adv Pharmacol. Vol. 93. pp. 373–401. doi:10.1016/bs.apha.2021.10.005. ISBN 978-0-323-91526-7. PMC 9826737. PMID 35341572. It is reported that methamphetamine (METH) interacts with TAAR1 and subsequently inhibits DA uptake, enhance DA efflux and induces DAT internalization, and these effects are dependent on TAAR1 (Xie & Miller, 2009). For example, METH-induced inhibition of DA uptake was observed in TAAR1 and DAT cotransfected cells and WT mouse and monkey striatal synaptosomes but not in DAT-only transfected cells or in striatal synaptosomes of TAAR1-KO mice (Xie & Miller, 2009). TAAR1 activation was enhanced by co-expression of monoamine transporters and this effect could be blocked by monoamine transporter antagonists (Xie & Miller, 2007; Xie et al., 2007). Furthermore, DA activation of TAAR1 induced C-FOS-luciferase expression only in the presence of DAT (Xie et al., 2007).
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  17. ^ Lewin AH, Miller GM, Gilmour B (December 2011). "Trace amine-associated receptor 1 is a stereoselective binding site for compounds in the amphetamine class". Bioorganic & Medicinal Chemistry. 19 (23): 7044–7048. doi:10.1016/j.bmc.2011.10.007. PMC 3236098. PMID 22037049. While our data suggest a role for TAAR1 in eliciting amphetamine-like stimulant effects, it must be borne in mind that the observed in vivo effects are likely to result from interaction with both TAAR1 and monoamine transporters. Thus it has been shown that the selective TAAR1 agonist RO5166017 fully prevented psychostimulant-induced and persistent hyperdopaminergia-related hyperactivity in mice.42 This effect was found to be DAT-independent, since suppression of hyperactivity was observed in DAT-KO mice.42 The collected information leads us to conclude that TAAR1 is a stereoselective binding site for amphetamine and that TAAR1 activation by amphetamine and its congeners may contribute to the stimulant properties of this class of compounds.
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  26. ^ Kuropka P, Zawadzki M, Szpot P (May 2023). "A narrative review of the neuropharmacology of synthetic cathinones-Popular alternatives to classical drugs of abuse". Hum Psychopharmacol. 38 (3): e2866. doi:10.1002/hup.2866. PMID 36866677. Another feature that distinguishes [substituted cathinones (SCs)] from amphetamines is their negligible interaction with the trace amine associated receptor 1 (TAAR1). Activation of this receptor reduces the activity of dopaminergic neurones, thereby reducing psychostimulatory effects and addictive potential (Miller, 2011; Simmler et al., 2016). Amphetamines are potent agonists of this receptor, making them likely to self‐inhibit their stimulating effects. In contrast, SCs show negligible activity towards TAAR1 (Kolaczynska et al., 2021; Rickli et al., 2015; Simmler et al., 2014, 2016). [...] The lack of self‐regulation by TAAR1 may partly explain the higher addictive potential of SCs compared to amphetamines (Miller, 2011; Simmler et al., 2013).
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