Social:Locomotor activity

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Locomotor activity is a measure of animal behavior which is employed in scientific research.[1][2]

Hyperlocomotion, also known as locomotor hyperactivity, hyperactivity, or increased locomotor activity, is an effect of certain drugs in animals in which locomotor activity (locomotion) is increased.[3] It is induced by certain drugs like psychostimulants and NMDA receptor antagonists and is reversed by certain other drugs like antipsychotics and certain antidepressants.[3][4][5][6] Stimulation of locomotor activity is thought to be mediated by increased signaling in the nucleus accumbens, a major brain area involved in behavioral activation and motivated behavior.[7][8][9][10]

Hypolocomotion, also known as locomotor hypoactivity, hypoactivity, and decreased locomotor activity, is an effect of certain drugs in animals in which locomotor activity is decreased.[11] It is a characteristic effect of many sedative agents and general anesthetics. Antipsychotics, which are dopamine receptor antagonists, and many serotonergic agents, such as meta-chlorophenylpiperazine (mCPP), can also produce this effect, often as a side effect. Although locomotor activity is mainly an animal behavior test, it has also been evaluated in humans.[1] People with attention deficit hyperactivity disorder (ADHD), in the manic phase of bipolar disorder, on acute amphetamine, and with schizophrenia show increased locomotor activity, while children with autism show decreased locomotor activity.[1] Conversely, reduced locomotor activity is observed in bipolar individuals on mood stabilizers[1] and may be a characteristic symptom of the inattentive type of ADHD[12] (ADHD-PI) and sluggish cognitive tempo.

Drugs affecting locomotor activity

Dopaminergic agents

Dopamine releasing agents

Hyperlocomotion is induced by dopamine releasing agents (DRAs) and psychostimulants like amphetamine and methamphetamine.[3][4][5][13][14] These drugs likewise induce stereotypies.[3][5]

Dopamine reuptake inhibitors

The dopamine reuptake inhibitors (DRIs) amineptine, bupropion, and nomifensine increase spontaneous locomotor activity in animals.[6][15] The DRI cocaine increases locomotor activity similarly to the preceding DRIs and to amphetamines.[13] The atypical DRI modafinil does not produce hyperlocomotion in animals.[13]

Dopamine receptor agonists

Direct dopamine receptor agonists like apomorphine show biphasic effects, decreasing locomotor activity at low doses and increasing locomotor activity at high doses.[7]

Dopamine receptor antagonists

Drug-induced hyperlocomotion can be reversed by various drugs, such as antipsychotics acting as dopamine D2 receptor antagonists.[3][5] Reversal of drug-induced hyperlocomotion has been used as an animal test of drug antipsychotic-like activity.[3][5] Reversal of amphetamine- and NMDA receptor antagonist-induced stereotypies is also employed as a test of drug antipsychotic-like activity.[3][5]

Adrenergic agents

Norepinephrine releasing agents

Selective norepinephrine releasing agents (NRAs) include ephedrine, pseudoephedrine, phenylpropanolamine, levomethamphetamine, and D-phenylalaninol.[16][17][18][19] However, these drugs also release dopamine to a much lesser extent (e.g., ~10-fold less potently).[16][17][18][19]

Ephedrine consistently stimulates locomotor activity in rodents.[20][21][22] However, the hyperlocomotion induced by ephedrine may be mediated by dopamine release rather than by norepinephrine release.[21][23] On the other hand, lesioning the brain noradrenergic system with the noradrenergic neurotoxin DSP-4 reduces dextroamphetamine-induced hyperlocomotion.[24][25] In addition, the selective α1-adrenergic receptor antagonist prazosin antagonizes amphetamine-induced hyperlocomotion[24][26] and knockout of the α1B-adrenergic receptor dramatically reduces dextroamphetamine-induced hyperlocomotion.[24][27] In contrast to ephedrine and amphetamine, pseudoephedrine[28][29] and phenylpropanolamine do not stimulate locomotor activity in rodents.[30][31][32] However, in another study, pseudoephedrine was able to increase locomotor activity.[22] A potential confounding factor with β-hydroxyamphetamines like phenylpropanolamine, ephedrine, and pseudoephedrine is that they have lower lipophilicity compared to their amphetamine counterparts, with consequent reduced capacity to cross the blood–brain barrier and produce central nervous system effects.[33][34][35][36]

Conversely, the potencies of monoamine releasing agents (MRAs) in producing amphetamine-type subjective effects in humans have been found to correlate with their potency to induce norepinephrine release and not with their potencies to induce dopamine release.[37][38] In addition, self-administration of methamphetamine appeared to be relatively resistant to blockade by dopamine receptor antagonists.[37] Findings on the modulation of the ventral tegmental area by the noradrenergic locus coeruleus are mixed and suggestive of both excitatory and inhibitory roles.[37] The α1-adrenergic receptor appears to be facilitatory, whereas the α2-adrenergic receptor appears to be inhibitory, and the β-adrenergic receptors appear to not be involved.[37] More research is needed to investigate the role of norepinephrine in dopamine modulation and stimulant-like effects.[37]

In contrast to normal mice, psychostimulants like amphetamine, β-phenethylamine, and methylphenidate lose their ability to elevate brain dopamine but not norepinephrine in dopamine transporter (DAT) knockout mice and have been found to decrease locomotor activity in these mice.[39][40][41][42] Paradoxically however, cocaine retains reinforcing effects in DAT knockout mice and cocaine and amphetamine are still able to elevate dopamine in the medial nucleus accumbens in these mice.[43] It was found that the norepinephrine reuptake inhibitor reboxetine increases dopamine levels in the nucleus accumbens in DAT knockout mice but not in normal mice, suggesting that the effects of norepinephrine elevation change in the brains of DAT knockout mice.[43]

Whereas dextromethamphetamine is a well-balanced norepinephrine–dopamine releasing agent (NDRA), levomethamphetamine is a selective NRA.[38][16][19][44] Levomethamphetamine has similar potency as an NRA compared to dextromethamphetamine.[45][13][46][47][16] Conversely, levomethamphetamine is about 15- to 20-fold less potent in inducing dopamine release than dextromethamphetamine.[16][19][44][38][46] In accordance with the preceding, levomethamphetamine was found to selectively induce brain norepinephrine release with minimal effect on brain dopamine release across an assessed dosage range in rodents.[48] The drug did not increase locomotor activity at the assessed doses, in which brain dopamine release was not affected.[48] In contrast to levomethamphetamine, dextromethamphetamine at the same doses increased brain levels of both norepinephrine and dopamine and induced dose-dependent hyperlocomotion.[48] Relatedly, levomethamphetamine shows similar sympathomimetic effects as dextromethamphetamine but is substantially less potent as a psychostimulant in animals.[49][50][51][48] As in rodents, levomethamphetamine showed reduced reinforcing and stimulant-like effects compared to dextromethamphetamine in rhesus monkeys.[52][53]

Animal studies of the reinforcing and cocaine-like effects of dopamine releasing agents (DRAs) with varying capacities to release norepinephrine and serotonin in rodents and monkeys have suggested that in contrast to the case of serotonin release, which inhibits the reinforcing and stimulant-like effects of these agents, norepinephrine release has minimal influence on their misuse liability and associated effects.[54][19][55]

Norepinephrine reuptake inhibitors

Norepinephrine reuptake inhibitors (NRIs), like atomoxetine, reboxetine, and desipramine, do not increase locomotor activity in rodents and instead show no effect on locomotor activity or decrease it.[56][57][58][59][60] In addition, NRIs decrease amphetamine-, cocaine-, methylphenidate-, and phencyclidine (PCP)-induced hyperlocomotion in rodents.[61][62] Accordingly, atomoxetine has been reported to attenuate the stimulant and rewarding effects of dextroamphetamine in humans.[63][64]

A variety of different NRIs were shown to decrease spontaneous locomotor activity in a novel environment when given acutely and to decrease locomotor activity in both novel and familiar environments when given chronically in rodents.[57] Similarly, norepinephrine transporter (NET) knockout mice had low basal locomotor activity.[57] However, combination of an NRI with dopamine reuptake inhibition resulted in increased locomotor activity.[57] It was concluded that norepinephrine reuptake inhibition by itself decreases locomotor activity unless it is combined with dopamine reuptake inhibition.[57]

Serotonergic agents

Serotonin releasing agents

Certain serotonin releasing agents (SRAs), like MDMA and MDAI, though notably not others, like chlorphentermine, fenfluramine, and MMAI,[65][17][66] induce locomotor hyperactivity in animals.[67][68][69][70] This is dependent on serotonin release allowed for by the serotonin transporter (SERT) and serotonin 5-HT2B receptor.[71][68][69][72][73] SERT knockout, pretreatment with serotonin reuptake inhibitors (SRIs) (which block MDMA-induced SERT-mediated serotonin release), or serotonin 5-HT2B receptor knockout (which likewise blocks MDMA-induced serotonin release), all completely block MDMA-induced locomotor hyperactivity.[71][68][69][72][73] In addition, locomotor hyperactivity produced by MDMA is partially attenuated by serotonin 5-HT1B receptor antagonism (or knockout)[71][74][75] or by serotonin 5-HT2A receptor antagonism.[76][77][78] The locomotor hyperactivity produced by MDMA is fully attenuated by combined serotonin 5-HT1B and 5-HT2A receptor antagonism.[77] Conversely, the serotonin 5-HT1A receptor is not involved in MDMA-induced hyperlocomotion.[68] Serotonin 5-HT2C receptor activation appears to inhibit MDMA-induced hyperlocomotion, and antagonism of this receptor has been reported to markedly enhance the locomotor hyperactivity induced by MDMA.[78][77][79][80] Activation of the serotonin 5-HT2C receptor is known to inhibit dopamine release in the mesolimbic pathway as well as to inhibit dopamine release in the nigrostriatal and mesocortical pathways.[81][82][78][83]

Although the serotonin system has been implicated in the hyperlocomotion of SRAs, certain SRAs, such as MDMA, are actually serotonin–norepinephrine–dopamine releasing agents (SNDRAs), and catecholaminergic mechanisms are likely to additionally be involved.[84][85] Relatedly, the α1-adrenergic receptor antagonist prazosin completely blocks MDMA-induced hyperlocomotion in animals.[86][85][87] In addition, the α1-adrenergic receptor antagonists prazosin and doxazosin reduce the psychostimulant and/or euphoric effects of MDMA in humans.[88][89][90] Similarly, the norepinephrine reuptake inhibitor (NRI) reboxetine, which prevents MDMA from inducing norepinephrine release, likewise reduces the stimulant effects and emotional excitation of MDMA in humans.[86][91] Dopamine receptors also appear to be involved in MDMA-induced hyperlocomotion, although findings in this area, both in animals and humans, seem to be conflicting.[86][92][93]

In contrast to non-selective SRAs like MDMA, the highly selective SRA MMAI induces hypolocomotion in animals.[94] Similarly, the highly selective SRA chlorphentermine is said to weakly stimulate locomotor activity at low doses and to progressively suppress locomotor activity at higher doses.[95]

The reasons for the differences in locomotor activity with different SRAs are not fully clear.[78] In any case, they may be related to factors such as whether the agents are selective SRAs, whether they additionally act as agonists of serotonin 5-HT2 receptors, and whether they additionally induce the release of norepinephrine and/or dopamine.[78][96][97][71][66][94]

Serotonin reuptake inhibitors

Selective serotonin reuptake inhibitors (SSRIs) have been reported to have no effect or to increase locomotor activity, at least under certain circumstances like novel environments.[97][57][58][60] However, in other studies, SSRIs have been reported to produce hypolocomotion, an effect that could be reversed by the serotonin 5-HT2C receptor antagonist SB-242084.[98][99][100] In another study, the SSRIs fluoxetine and citalopram had no effect on locomotor activity alone or in combination with SB-242084.[97]

Fluoxetine has been found to not affect dextroamphetamine-induced hyperlocomotion.[61] Similarly, sertraline did not affect cocaine-induced hyperlocomotion.[101]

Serotonin precursors

The serotonin precursor 5-hydroxytryptophan (5-HTP) combined with benserazide can suppress the hyperlocomotion induced by dextroamphetamine in rodents.[102]

Serotonin receptor agonists

The non-selective serotonin receptor agonists and serotonergic psychedelics LSD and DOI decrease locomotor activity in animals.[14] However, whereas LSD suppresses locomotion at all doses tested, DOI as well as DOM show an inverted U-shaped dose–response curve, with stimulation of locomotor activity at low doses and suppression of locomotion at higher doses.[14][103][104][105][106] The hyperlocomotion of DOI at low doses is abolished in serotonin 5-HT2A receptor knockout mice, whereas the hypolocomotion with DOI at higher doses is blocked by the selective serotonin 5-HT2C receptor antagonist SER-082.[14][103][105] Similarly, the hyperlocomotion of low doses of DOM is reduced by the serotonin 5-HT2A receptor antagonist volinanserin (MDL-100907) and enhanced by the serotonin 5-HT2C receptor antagonist SB-242084 and its hypolocomotion at high doses is attenuated by SB-242084.[104] As such, it has been concluded that serotonin 5-HT2A receptor activation increases locomotor activity while serotonin 5-HT2C receptor agonism decreases locomotor activity.[103][104][106]

The locomotor effects of many other serotonergic psychedelics have also been studied and have often been similar to the preceding agents.[105] However, in other cases, they have been different.[105] The tryptamine psychedelics psilocin and 5-MeO-DMT produce profound hypolocomotion in mice and this is blocked by the serotonin 5-HT1A receptor antagonist WAY-100635 or by serotonin 5-HT1A receptor knockout but not by the serotonin 5-HT2C receptor antagonist SB-242084.[105] 5-MeO-DALT dose-dependently increased locomotor activity but produced a sharp decrease at the highest tested dose.[107] The relatively selective serotonin 5-HT2A receptor agonist 25I-NBOMe has been found to show similar locomotor effects to phenylalkylamine psychedelics, increasing locomotor activity at low doses at decreasing it at higher doses.[106][107] The selective serotonin 5-HT2A receptor agonist 25CN-NBOH modestly increased locomotor activity or did not affect it.[108][109][110]

The non-selective serotonin 5-HT2C receptor agonists meta-chlorophenylpiperazine (mCPP) and Ro60-0175 as well as the selective serotonin 5-HT2C receptor agonists WAY-161503 and CP-809101 produce hypolocomotion in rodents.[97][111][105] In serotonin 5-HT2C receptor knockout mice, on the other hand, mCPP produced hyperlocomotion.[97] In contrast to most serotonin 5-HT2C receptor agonists, the selective serotonin 5-HT2C receptor agonist WAY-163909 had no effect on spontaneous locomotor activity.[111] The selective serotonin 5-HT2C receptor agonists WAY-163909 and CP-809101 have been found to suppress dextroamphetamine-induced hyperlocomotion.[111][112] The non-selective serotonin 5-HT2C receptor agonist Ro60-0175 has been found to suppress the hyperlocomotion induced by cocaine, and this effect could be blocked by the selective serotonin 5-HT2C receptor antagonist SB-242084.[97] CP-809101 has been found to decrease locomotor activity and antagonized phencyclidine (PCP)-induced hyperlocomotion.[112]

Serotonin receptor antagonists

Serotonin 5-HT2A receptor antagonists like volinanserin (MDL-100907) and ketanserin counteract the hyperactivity induced by amphetamine, cocaine, and NMDA receptor antagonists like PCP in animals.[113][14][114][115][116][117][118][119] Less-selective serotonin 5-HT2A receptor antagonists, like trazodone, have been found to decrease locomotor and behavioral activity and to inhibit amphetamine-, cocaine-, and PCP-induced hyperactivity in animals similarly.[116][120][121][122][123][6] Blockade of the serotonin 5-HT2A receptor by atypical antipsychotics like clozapine and olanzapine contributes to the hypolocomotion they produce.[105][124] In addition to serotonin 5-HT2A receptor antagonists, serotonin 5-HT2A receptor biased agonists that selectively activate the β-arrestin pathway but not the Gq pathway, like 25N-N1-Nap, have been found to antagonize PCP-induced locomotor hyperactivity in rodents.[113]

Serotonin 5-HT2B receptor antagonists by themselves do not appear to affect locomotor activity.[125] However, antagonists of the serotonin 5-HT2B receptor decrease the locomotor hyperactivity of amphetamine, cocaine, and phencyclidine (PCP).[126][127][128][129]

The selective serotonin 5-HT2C receptor antagonist SB-242084 has been found to produce modest hyperlocomotion at high doses in rodents.[130][131][105] The drug has also been found to produce modest stimulant-like effects in squirrel monkeys.[130] SB-242084 has additionally been found to enhance the hyperlocomotion of dextroamphetamine in rodents.[111] Similarly, it has been found to dose-dependently enhance the hyperlocomotion induced by dexfenfluramine in rodents.[97][132] It has also been found to enhance the hyperlocomotion induced by MDMA, fenfluramine, cocaine, and methylphenidate, to modestly enhance nicotine- and morphine-induced hyperactivity, and to not affect the hyperactivity induced by RU-24969 or citalopram.[133] The serotonin 5-HT2C receptor antagonist SB-221284 has been found to augment the nucleus accumbens dopamine elevations and hyperlocomotion induced by NMDA receptor antagonists like phencyclidine (PCP) and dizocilpine (MK-801) in rodents.[134]

Glutamatergic agents

NMDA receptor antagonists

Hyperlocomotion is induced by NMDA receptor antagonists and dissociative hallucinogens such as phencyclidine (PCP), ketamine, and dizocilpine (MK-801).[3][4][5][13][14] These drugs likewise induce stereotypies.[3][5]

Cholinergic agents

Muscarinic acetylcholine receptor antagonists

Non-selective muscarinic acetylcholine receptor antagonists, or antimuscarinics, such as atropine, hyoscyamine, and scopolamine, produce robust hyperactivity in animals, but also produce deliriant effects such as amnesia and hallucinations in both animals and humans.[135][136]

Cannabinoids

Tetrahydrocannabinol (THC) produces hypolocomotion in rodents.[137] Cannabidiol (CBD) does not appear to affect locomotor activity when administered by itself or when added to THC.[137] However, in some studies, CBD augmented THC-induced hypolocomotion.[137]

Opioids

Classical opioids or μ-opioid receptor agonists like morphine and fentanyl stimulate locomotor activity in rodents.[138][139][140] However, high doses of μ-opioid receptor agonists induce locomotor depression.[141] δ-Opioid receptor agonists like AZD-2327 likewise stimulate locomotor activity in rodents.[142][143]

TAAR1 modulators

The trace amine-associated receptor 1 (TAAR1) regulates the monoaminergic system and is a biological target for trace amines like β-phenethylamine and tyramine, the thyronamine 3-iodothyronamine, and drugs like amphetamines.[144][145]

TAAR1 knockout mice show unchanged basal locomotor activity.[146] However, they show enhanced hyperlocomotion with amphetamine, methamphetamine, and MDMA, as well as with β-phenethylamine.[147][148][149] TAAR1 overexpression likewise is associated with unchanged basal locomotor activity.[150] However, overexpression of the TAAR1 results in only weak locomotor stimulation by amphetamine.[147][151][152][153] The TAAR1 full agonists RO5256390, ulotaront (SEP-363856), and LK00764 have been found to suppress locomotion in mice.[154][155][156] Conversely, the TAAR1 full agonist RO5166017[157][158] and the TAAR1 partial agonists RO5073012,[153] RO5203648,[159] and RO5263397 on their own did not affect basal locomotion in rodents.[160][161][162] Similarly, the TAAR1 partial agonist RO5263397 did not affect locomotor activity in monkeys.[163] The TAAR1 antagonist EPPTB does not affect basal locomotor activity in rodents.[158][164]

The TAAR1 full agonists RO5166017, RO5256390, and ulotaront all suppress psychostimulant-induced hyperlocomotion in mice.[147][165][166] The TAAR1 partial agonists RO5073012, RO5203648, and RO5263397 suppress locomotor stimulation induced by cocaine.[147][151][165][167] The TAAR1 partial agonist RO5203648 suppressed dextroamphetamine-induced hyperlocomotion at the highest assessed dose in rats but did not affect dextroamphetamine-induced hyperactivity in mice.[152][166][150][159] It showed complex effects on methamphetamine-induced hyperlocomotion in rats, reducing early but potentiating late methamphetamine-induced hyperlocomotion with acute administration and suppressing methamphetamine-induced hyperlocomotion with chronic administration.[152][168] The dual TAAR1 full agonist and serotonin 5-HT1 receptor modulator ulotaront did not affect dextroamphetamine-induced hyperlocomotion in rats.[169] The TAAR1 weak partial agonist RO5073012 did not affect amphetamine-induced hyperlocomotion in mice but substantially restored the locomotor stimulation of amphetamine in mice with TAAR1 overexpression.[152][151][153] In an unpublished study, EPPTB was reported to considerably reduce methamphetamine-induced hyperlocomotion in mice chronically exposed to methamphetamine, an effect that was absent in TAAR1 knockout mice.[170][171] The TAAR1 full agonists RO5166017, RO5256390, ulotaront, and LK00764 and the TAAR1 partial agonists RO5203648 and RO5263397 suppress the hyperlocomotion induced by NMDA receptor antagonists like phencyclidine (PCP), L-687,414, and dizocilpine (MK-801) in rodents.[152][157][167][172][156]

Other agents

Many tricyclic antidepressants (TCAs) do not increase locomotion, and instead often actually show behavioral sedation.[6][7][173]

Non-drug stimuli affecting locomotor activity

Light exposure has been found to increase locomotor activity and exploratory behavior in rodents.[174]

Similar behavioral measures

Other similar behavioral measures include stereotypy, exploratory behavior, climbing behavior, and jumping behavior.[175][4][5] Amphetamines, which are dopamine releasing agents (DRAs) induce stereotypies in addition to hyperlocomotion.[4][5] The dopamine receptor agonist apomorphine induces stereotypy and climbing behavior.[4] The dopamine precursor levodopa (L-DOPA) induces jumping behavior.[4] These effects can all be reversed by antipsychotics, which are dopamine receptor antagonists.[4]

See also

References

  1. ↑ 1.0 1.1 1.2 1.3 "Locomotor Profiling from Rodents to the Clinic and Back Again". Translational Neuropsychopharmacology. Current Topics in Behavioral Neurosciences. 28. 2016. pp. 287–303. doi:10.1007/7854_2015_5015. ISBN 978-3-319-33911-5. 
  2. ↑ "Measuring Locomotor Activity and Behavioral Aspects of Rodents Living in the Home-Cage". Front Behav Neurosci 16. 2022. doi:10.3389/fnbeh.2022.877323. PMID 35464142. 
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 Castagné, Vincent; Moser, Paul C.; Porsolt, Roger D. (2009). "Preclinical Behavioral Models for Predicting Antipsychotic Activity". Advances in Pharmacology. 57. Elsevier. pp. 381–418. doi:10.1016/s1054-3589(08)57010-4. ISBN 978-0-12-378642-5. 
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 "Animal models for the evaluation of antipsychotic agents". Fundam Clin Pharmacol 37 (3): 447–460. June 2023. doi:10.1111/fcp.12855. PMID 36410728. 
  5. ↑ 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 "A conceptual and practical guide to the behavioural evaluation of animal models of the symptomatology and therapy of schizophrenia". Cell Tissue Res 354 (1): 221–246. October 2013. doi:10.1007/s00441-013-1611-0. PMID 23579553. 
  6. ↑ 6.0 6.1 6.2 6.3 "The effects of tricyclic and 'atypical' antidepressants on spontaneous locomotor activity in rodents". Neurosci Biobehav Rev 10 (2): 115–121. 1986. doi:10.1016/0149-7634(86)90022-9. PMID 3737024. 
  7. ↑ 7.0 7.1 7.2 "The role of dopamine in the mechanism of action of antidepressant drugs". Eur J Pharmacol 405 (1–3): 365–373. September 2000. doi:10.1016/s0014-2999(00)00566-5. PMID 11033341. 
  8. ↑ "The role of nucleus accumbens dopamine in motivated behavior: a unifying interpretation with special reference to reward-seeking". Brain Res Brain Res Rev 31 (1): 6–41. December 1999. doi:10.1016/s0165-0173(99)00023-5. PMID 10611493. 
  9. ↑ "Mesolimbic Dopamine and the Regulation of Motivated Behavior". Behavioral Neuroscience of Motivation. Current Topics in Behavioral Neurosciences. 27. 2016. pp. 231–257. doi:10.1007/7854_2015_383. ISBN 978-3-319-26933-7. 
  10. ↑ "The Neurobiology of Activational Aspects of Motivation: Exertion of Effort, Effort-Based Decision Making, and the Role of Dopamine". Annu Rev Psychol 75: 1–32. January 2024. doi:10.1146/annurev-psych-020223-012208. PMID 37788571. 
  11. ↑ "APA Dictionary of Psychology" (in en). https://dictionary.apa.org/. 
  12. ↑ Diagnostic and statistical manual of mental disorders: DSM-5. Arlington, VA: American Psychiatric Association. 2013. ISBN 978-0-89042-554-1. http://archive.org/details/diagnosticstatis0005unse. 
  13. ↑ 13.0 13.1 13.2 13.3 13.4 "Modes of Action of Drugs Related to Narcolepsy: Pharmacology of Wake-Promoting Compounds and Anticataplectics". Narcolepsy: A Clinical Guide (2nd ed.). Cham: Springer International Publishing. 2016. pp. 307–329. doi:10.1007/978-3-319-23739-8_22. ISBN 978-3-319-23738-1. https://www.researchgate.net/publication/314626865. 
  14. ↑ 14.0 14.1 14.2 14.3 14.4 14.5 "Animal models of serotonergic psychedelics". ACS Chem Neurosci 4 (1): 33–42. January 2013. doi:10.1021/cn300138m. PMID 23336043. 
  15. ↑ Rampello, Liborio; Nicoletti, Ferdinando; Nicoletti, Francesco (2000). "Dopamine and Depression". CNS Drugs (Springer Science and Business Media LLC) 13 (1): 35–45. doi:10.2165/00023210-200013010-00004. ISSN 1172-7047. 
  16. ↑ 16.0 16.1 16.2 16.3 16.4 "Monoamine transporters and psychostimulant drugs". European Journal of Pharmacology 479 (1–3): 23–40. October 2003. doi:10.1016/j.ejphar.2003.08.054. PMID 14612135. 
  17. ↑ 17.0 17.1 17.2 "Therapeutic potential of monoamine transporter substrates". Current Topics in Medicinal Chemistry 6 (17): 1845–1859. 2006. doi:10.2174/156802606778249766. PMID 17017961. 
  18. ↑ 18.0 18.1 "In vitro characterization of ephedrine-related stereoisomers at biogenic amine transporters and the receptorome reveals selective actions as norepinephrine transporter substrates". J Pharmacol Exp Ther 307 (1): 138–145. October 2003. doi:10.1124/jpet.103.053975. PMID 12954796. 
  19. ↑ 19.0 19.1 19.2 19.3 19.4 "Cocaine-like discriminative stimulus effects of "norepinephrine-preferring" monoamine releasers: time course and interaction studies in rhesus monkeys". Psychopharmacology (Berl) 234 (23–24): 3455–3465. December 2017. doi:10.1007/s00213-017-4731-5. PMID 28889212. "In the present experiments, two monoamine releasers, l-MA and PAL-329, were shown to produce cocaine-like discriminative-stimulus effects in monkeys, suggesting that they meet the above criteria. One of these compounds, l-MA, also has been shown to serve as a positive reinforcer in rodents (Yokel and Pickens 1973) and monkeys (Winger et al 1994), further confirming the overlap with behavioral effects of cocaine. Both compounds also exhibit an approximately 15-fold greater potency in releasing NE than DA, which may be therapeutically advantageous. For example, the subjective effects of l-MA in human studies are similar in some respects to those of d-MA. However, the subjective effects of the two isomers also differ in potentially important ways. While both l-MA and d-MA produce subjective ratings of "drug liking" and "good effects" in experienced stimulant users, only l-MA produces concomitant ratings of bad or aversive drug effects (Mendelson et al 2006), a factor which may limit its abuse liability.". 
  20. ↑ "Pharmacokinetics and locomotor activity increasing effect of ephedrine in mice". Acta Pharmacol Toxicol (Copenh) 43 (5): 381–386. November 1978. doi:10.1111/j.1600-0773.1978.tb02282.x. PMID 726903. 
  21. ↑ 21.0 21.1 "Dopamine-like properties of ephedrine in rat brain". Br J Pharmacol 74 (1): 119–122. September 1981. doi:10.1111/j.1476-5381.1981.tb09962.x. PMID 7196787. 
  22. ↑ 22.0 22.1 "The effect of ephedrine isomers and their oxazolidines on locomotor activity in rats". Gen Pharmacol 24 (3): 669–673. May 1993. doi:10.1016/0306-3623(93)90229-q. PMID 8365649. 
  23. ↑ "Effects of (-)-ephedrine on locomotion, feeding, and nucleus accumbens dopamine in rats". Psychopharmacology (Berl) 135 (2): 133–140. January 1998. doi:10.1007/s002130050494. PMID 9497018. 
  24. ↑ 24.0 24.1 24.2 "There and back again: a tale of norepinephrine and drug addiction". Neuropsychopharmacology 32 (7): 1433–1451. July 2007. doi:10.1038/sj.npp.1301263. PMID 17164822. 
  25. ↑ "Evidence for a selective brain noradrenergic involvement in the locomotor stimulant effects of amphetamine in the rat". Neurosci Lett 43 (2–3): 327–31. December 1983. doi:10.1016/0304-3940(83)90209-4. PMID 6687006. 
  26. ↑ "Prazosin: effect on psychomotor-stimulant cues and locomotor activity in mice". Eur J Pharmacol 116 (3): 221–228. October 1985. doi:10.1016/0014-2999(85)90156-6. PMID 3878298. 
  27. ↑ "Alpha1b-adrenergic receptors control locomotor and rewarding effects of psychostimulants and opiates". J Neurosci 22 (7): 2873–2884. April 2002. doi:10.1523/JNEUROSCI.22-07-02873.2002. PMID 11923452. 
  28. ↑ "[Effect of d-pseudoephedrine on the central nervous system in mice]" (in Japanese). Nihon Yakurigaku Zasshi 79 (5): 401–408. May 1982. doi:10.1254/fpj.79.401. PMID 6813205. 
  29. ↑ "Local field potential power spectra and locomotor activity following treatment with pseudoephedrine in mice". Acta Neurobiol Exp (Wars) 80 (1): 19–31. 2020. doi:10.21307/ane-2020-002. PMID 32214271. 
  30. ↑ "A comparison of the effects of phenylpropanolamine, d-amphetamine and d-norpseudoephedrine on open-field locomotion and food intake in the rat". Appetite 9 (1): 31–37. August 1987. doi:10.1016/0195-6663(87)90051-1. PMID 3662492. 
  31. ↑ "Self-administration of phenylpropanolamine (PPA) by rats previously trained to self-administer amphetamine". Pharmacol Biochem Behav 34 (1): 187–191. September 1989. doi:10.1016/0091-3057(89)90371-7. PMID 2626448. 
  32. ↑ "The pharmacology of the anorexic effect of phenylpropanolamine". Drugs Exp Clin Res 16 (9): 487–495. 1990. PMID 2100250. 
  33. ↑ "Pharmacokinetics of non-prescription sympathomimetic agents". Biopharm Drug Dispos 10 (1): 1–14. 1989. doi:10.1002/bdd.2510100102. PMID 2647163. 
  34. ↑ "Informed decision-making on sympathomimetic use in sport and health". Clin J Sport Med 12 (4): 209–224. July 2002. doi:10.1097/00042752-200207000-00003. PMID 12131054. 
  35. ↑ "Why Are the Majority of Active Compounds in the CNS Domain Natural Products? A Critical Analysis". J Med Chem 61 (23): 10345–10374. December 2018. doi:10.1021/acs.jmedchem.7b01922. PMID 29989814. 
  36. ↑ "The clinical toxicology of metamfetamine". Clin Toxicol (Phila) 48 (7): 675–694. August 2010. doi:10.3109/15563650.2010.516752. PMID 20849327. "Metamfetamine acts in a manner similar to amfetamine, but with the addition of the methyl group to the chemical structure. It is more lipophilic (Log p value 2.07, compared with 1.76 for amfetamine),4 thereby enabling rapid and extensive transport across the blood–brain barrier.19". 
  37. ↑ 37.0 37.1 37.2 37.3 37.4 Bauer, Clayton T. (5 July 2014). "Determinants of Abuse-Related Effects of Monoamine Releasers in Rats". https://scholarscompass.vcu.edu/etd/522/. "Another potential determinant for increased abuse potential of MARs is selectivity for DA versus NE. Although DA is well-established to be a key neurotransmitter in mediating abuse-related effects of monoamine releasers and other drugs (for review, Leshner and Koob, 1999), amphetamine and other abused monoamine releasers have slightly (2 to 3x) higher potency to release NE than DA (Rothman et al., 2001). Moreover, methamphetamine self-administration in rats was relatively resistant to pretreatment with DA-antagonists (Brennan et al., 2009), and ephedrine (a 19-fold NE-selective releaser) has been shown to maintain self-administration in monkeys (Anderson et al., 2001) and substitute for amphetamine (Young et al., 1998) and methamphetamine (Bondareva et al., 2002) in drug discrimination studies in rats. Perhaps the most compelling data on the importance of NE comes from human subjects where amphetamine-like discriminative stimuli produced by monoamine releasers correlate with potency to release NE, not DA (Rothman et al., 2001). [...] There is also evidence of noradrenergic innervation of the dopaminergic system (Geisler and Zahm, 2005; Jones and Moore, 1977). Electrical stimulation of the locus coeruleus (LC) neurons increased levels of NE in the VTA and increased activity of DA neurons (Grenhoff et al., 1993). However, when exogenous NE was applied to the VTA, a decrease in firing rates of DA neurons was seen (Aghajanian and Bunney, 1977; White and Wang, 1984). Similar to the results of the latter study, lesions of the NE system by injection of 6-OHDA into the locus coeruleus increased firing of DA neurons in the VTA by 70% (Guiard et al., 2008). These data suggest that there may be both excitatory and inhibitory roles of NE on the activity of VTA dopaminergic neurons. [...] The receptors by which NE modulates DA at the level of the VTA are fairly well characterized. In particular, it appears that the α-1 receptor is responsible for increases in DA neuron firing following NE administration while the α-2 receptor mediates the inhibitory effects of NE (Grenhoff and Svensson, 1988; Grenhoff and Svensson 1989; Grenhoff and Svensson, 1993; Grenhoff et al., 1995). In addition to the α-2 receptor, it appears that NE can act directly on D2 dopaminergic autoreceptors to produce inhibitory effects (Grenhoff et al., 1995; Lacey et al., 1987; Arencibia-Albite et al., 2007; Guiard et al., 2008). ß-adrenoreceptors are not known to exist in the VTA (Grenhoff et al., 1995; Jones et al., 1990) and ß-adrenergic compounds do not mediate the effects of NE in the VTA (Grenhoff et al., 1995)." 
  38. ↑ 38.0 38.1 38.2 "Amphetamine-type central nervous system stimulants release norepinephrine more potently than they release dopamine and serotonin". Synapse 39 (1): 32–41. January 2001. doi:10.1002/1098-2396(20010101)39:1<32::AID-SYN5>3.0.CO;2-3. PMID 11071707. 
  39. ↑ "Dopamine Dysregulation and Altered Responses to Drugs Affecting Dopaminergic Transmission in a New Dopamine Transporter Knockout (DAT-KO) Rat Model". Neuroscience 491: 43–64. May 2022. doi:10.1016/j.neuroscience.2022.03.019. PMID 35331847. 
  40. ↑ "Pronounced Hyperactivity, Cognitive Dysfunctions, and BDNF Dysregulation in Dopamine Transporter Knock-out Rats". J Neurosci 38 (8): 1959–1972. February 2018. doi:10.1523/JNEUROSCI.1931-17.2018. PMID 29348190. 
  41. ↑ "Dopamine transporter-dependent and -independent actions of trace amine beta-phenylethylamine". J Neurochem 91 (2): 362–373. October 2004. doi:10.1111/j.1471-4159.2004.02721.x. PMID 15447669. 
  42. ↑ "Hyperlocomotion and indifference to cocaine and amphetamine in mice lacking the dopamine transporter". Nature 379 (6566): 606–612. February 1996. doi:10.1038/379606a0. PMID 8628395. Bibcode: 1996Natur.379..606G. 
  43. ↑ 43.0 43.1 "Cocaine and amphetamine increase extracellular dopamine in the nucleus accumbens of mice lacking the dopamine transporter gene". J Neurosci 21 (9): RC141: 1–4. May 2001. doi:10.1523/JNEUROSCI.21-09-j0001.2001. PMID 11312315. 
  44. ↑ 44.0 44.1 "Human pharmacology of the methamphetamine stereoisomers". Clin Pharmacol Ther 80 (4): 403–420. October 2006. doi:10.1016/j.clpt.2006.06.013. PMID 17015058. "The stereoisomers of methamphetamine produce markedly different dopamine, norepinephrine, and serotonin responses in various brain regions in rats.41,42 d-Methamphetamine (2 mg/kg) is more potent in releasing caudate dopamine than l-methamphetamine (12 and 18 mg/kg). By use of in vitro uptake and release assays, d-methamphetamine (50% effective concentration [EC50], 24.5 ± 2.1 nmol/L) was 17 times more potent in releasing dopamine than l-methamphetamine (EC50, 416 ± 20 nmol/L) and significantly more potent in blocking dopamine uptake (inhibition constant [Ki ], 114 ± 11 nm versus 4840 ± 178 nm).12,13". 
  45. ↑ "Amphetamine, past and present--a pharmacological and clinical perspective". J Psychopharmacol 27 (6): 479–496. June 2013. doi:10.1177/0269881113482532. PMID 23539642. 
  46. ↑ 46.0 46.1 "Further pharmacological comparison of D-methamphetamine and L-methamphetamine in rats: abuse-related behavioral and physiological indices". Behav Pharmacol 30 (5): 422–428. August 2019. doi:10.1097/FBP.0000000000000453. PMID 30480551. "When considered with neurochemical data that l-MA is similarly potent in releasing norepinephrine (NE) but 15- to 20-fold less potent in releasing dopamine (DA), as compared to d-MA (Kuczenski et al., 1995; Melega et al., 1999), l-MA may appear to carry lower abuse liability than d-MA.". 
  47. ↑ "Hippocampus norepinephrine, caudate dopamine and serotonin, and behavioral responses to the stereoisomers of amphetamine and methamphetamine". The Journal of Neuroscience 15 (2): 1308–1317. February 1995. doi:10.1523/jneurosci.15-02-01308.1995. PMID 7869099. "Consistent with our past results, in response to 2 mg/kg D-AMPH, mean caudate extracellular DA increased approximately 15-fold to a peak concentration of 688 ± 121 nM during the initial 20 min interval, then returned to baseline over the next 3 hr. Similarly, in response to 2 mg/kg D-METH, DA increased to a peak concentration of 648 ± 71 nM during the initial 20 min interval and then declined toward baseline. In contrast, in response to both 6 mg/kg L-AMPH and 12 mg/kg L-METH, peak DA concentrations (508 ± 51 and 287 ± 49 nM, respectively) were delayed to the second 20 min interval, before returning toward baseline. [...] Similar to our previous results, 2 mg/kg D-AMPH increased NE to a maximum of 29.3 ± 3.1 nM, about 20-fold over baseline, during the second 20 min interval. L-AMPH (6 mg/kg) produced a comparable effect, increasing NE concentrations to 32.0 ± 8.9 nM. In contrast, D-METH promoted an increase in NE to 12.0 ± 1.2 nM which was significantly lower than all other groups, whereas L-METH promoted an increase to 64.8 ± 4.9 nM, which was significantly higher than all other groups.". 
  48. ↑ 48.0 48.1 48.2 48.3 "Distinct Effects of Methamphetamine Isomers on Limbic Norepinephrine and Dopamine Transmission in the Rat Brain". ACS Chem Neurosci. March 2023. doi:10.1021/acschemneuro.2c00689. PMID 36976755. 
  49. ↑ Biel, J. H.; Bopp, B. A. (1978). "Amphetamines: Structure-Activity Relationships". Stimulants. Boston, MA: Springer US. pp. 1–39. doi:10.1007/978-1-4757-0510-2_1. ISBN 978-1-4757-0512-6. "The configuration of the α-methyl group is also an important determinant of the stimulant activity. The dextro isomers of both amphetamine and methamphetamine are considerably more potent as stimulants than the levo isomers. Depending on the parameter measured, the potency difference may range from two- to tenfold (Taylor and Snyder, 1970; Snyder et at., 1970b; Svensson, 1971; Roth et at., 1954; Van Rossum, 1970; Moore, 1963). The anorexic activity of the dextro isomers also exceeds that of the levo isomers (Lawlor et at., 1969). However, the two isomers are approximately equipotent in eliciting certain peripheral effects, such as the vasoconstriction, vasopressor, and other cardiovascular effects (Roth et at., 1954; Swanson et at., 1943)." 
  50. ↑ "Psychomotor effect differences between l-methamphetamine and d-methamphetamine are independent of murine plasma and brain pharmacokinetics profiles". J Neural Transm (Vienna) 124 (5): 519–523. May 2017. doi:10.1007/s00702-017-1694-y. PMID 28213761. "There have been no studies directly comparing the pharmacodynamics and pharmacokinetics of the methamphetamine enantiomers in mice. It is often suggested that dmethamphetamine exerts more potent physiological and pharmacological effects than l-methamphetamine does, and that the stimulating effects exerted by l-methamphetamine on the central nervous system are 2–10 times less potent than those of d-methamphetamine (Mendelson et al. 2006). The results of the present study indicated that psychostimulant effects induced by l-methamphetamine are lower than those elicited by one-tenth the dose of d-methamphetamine. In addition, plasma pharmacokinetic parameters and striatal concentrations of methamphetamine following administration of l-methamphetamine at 10 mg/ kg (which did not induce psychomotor activity) were approximately 11 and 16 times as high, respectively, as those following administration of 1 mg/kg d-methamphetamine. Despite the fact that there are differentiable psycho-stimulating effects between two enantiomers, no significant difference in plasma pharmacokinetic parameters was detected at 1 mg/kg.". 
  51. ↑ "Comparison of some behavioral effects of d- and l-methamphetamine in adult male rats". Psychopharmacology (Berl) 234 (14): 2167–2176. July 2017. doi:10.1007/s00213-017-4623-8. PMID 28386698. 
  52. ↑ "Reinforcing and Stimulant-Like Effects of Methamphetamine Isomers in Rhesus Macaques". J Pharmacol Exp Ther 378 (2): 124–132. August 2021. doi:10.1124/jpet.121.000548. PMID 33986037. 
  53. ↑ "Effects of L-methamphetamine treatment on cocaine- and food-maintained behavior in rhesus monkeys". Psychopharmacology (Berl) 233 (6): 1067–1075. March 2016. doi:10.1007/s00213-015-4186-5. PMID 26713332. 
  54. ↑ "Abuse-related effects of dual dopamine/serotonin releasers with varying potency to release norepinephrine in male rats and rhesus monkeys". Exp Clin Psychopharmacol 22 (3): 274–284. June 2014. doi:10.1037/a0036595. PMID 24796848. 
  55. ↑ de Moura, Fernando Barreto; Sherwood, Alexander; Prisinzano, Thomas Edward; Kohut, Stephen John; Bergman, Jack (2018). "Intravenous Self-Administration of Synthetic Cathinones in Rhesus Monkeys". The FASEB Journal 32 (S1). doi:10.1096/fasebj.2018.32.1_supplement.550.3. ISSN 0892-6638. 
  56. ↑ "A review of the abuse potential assessment of atomoxetine: a nonstimulant medication for attention-deficit/hyperactivity disorder". Psychopharmacology (Berl) 226 (2): 189–200. March 2013. doi:10.1007/s00213-013-2986-z. PMID 23397050. 
  57. ↑ 57.0 57.1 57.2 57.3 57.4 57.5 "The effects of norepinephrine transporter inactivation on locomotor activity in mice". Biol Psychiatry 60 (10): 1046–1052. November 2006. doi:10.1016/j.biopsych.2006.03.057. PMID 16893531. 
  58. ↑ 58.0 58.1 "The effects of serotonin reuptake inhibitors on locomotor activity in gerbils". Pharmacol Biochem Behav 85 (1): 44–49. September 2006. doi:10.1016/j.pbb.2006.07.005. PMID 16920181. 
  59. ↑ "Pharmacological profile of reboxetine, a representative of new class of antidepressant drugs, selective noradrenaline reuptake inhibitor (NARI), given acutely". Pol J Pharmacol 51 (5): 399–404. 1999. PMID 10817540. 
  60. ↑ 60.0 60.1 "Induction of hyperlocomotion in mice exposed to a novel environment by inhibition of serotonin reuptake. A pharmacological characterization of diverse classes of antidepressant agents". Pharmacol Biochem Behav 71 (4): 667–680. April 2002. doi:10.1016/s0091-3057(01)00701-8. PMID 11888558. 
  61. ↑ 61.0 61.1 "Norepinephrine uptake inhibitors as biochemically and behaviorally selective antagonists of the locomotor stimulation induced by indirectly acting sympathomimetic aminetic amines in mice". Psychopharmacology (Berl) 69 (1): 27–34. 1980. doi:10.1007/BF00426517. PMID 6771822. 
  62. ↑ "Modulation of MK-801-induced behaviour by noradrenergic agents in mice". Psychopharmacology (Berl) 154 (2): 177–188. March 2001. doi:10.1007/s002130000630. PMID 11314680. 
  63. ↑ "Promising medications for cocaine dependence treatment". Recent Pat CNS Drug Discov 6 (2): 146–160. May 2011. doi:10.2174/157488911795933893. PMID 21599628. 
  64. ↑ "Atomoxetine attenuates dextroamphetamine effects in humans". Am J Drug Alcohol Abuse 35 (6): 412–6. 2009. doi:10.3109/00952990903383961. PMID 20014909. 
  65. ↑ "Dual dopamine-5-HT releasers: potential treatment agents for cocaine addiction". Trends Pharmacol Sci 27 (12): 612–618. December 2006. doi:10.1016/j.tips.2006.10.006. PMID 17056126. 
  66. ↑ 66.0 66.1 "Suppression of behavioral activity by norfenfluramine and related drugs in rats is not mediated by serotonin release". Psychopharmacology (Berl) 111 (2): 169–178. 1993. doi:10.1007/BF02245519. PMID 7870948. 
  67. ↑ Callaway, C. W.; Nichols, D. E.; Paulus, M. P.; Geyer, M. A. (1991). "Serotonin Release is Responsible for the Locomotor Hyperactivity in Rats Induced by Derivatives of Amphetamine Related to MDMA". Serotonin: Molecular Biology, Receptors and Functional Effects. Basel: Birkhäuser Basel. pp. 491–505. doi:10.1007/978-3-0348-7259-1_49. ISBN 978-3-0348-7261-4. 
  68. ↑ 68.0 68.1 68.2 68.3 "Mice in ecstasy: advanced animal models in the study of MDMA". Curr Pharm Biotechnol 11 (5): 421–433. August 2010. doi:10.2174/138920110791591508. PMID 20420576. 
  69. ↑ 69.0 69.1 69.2 "Of mice and men on MDMA: A translational comparison of the neuropsychobiological effects of 3,4-methylenedioxymethamphetamine ('Ecstasy')". Brain Res 1727. January 2020. doi:10.1016/j.brainres.2019.146556. PMID 31734398. 
  70. ↑ "Pharmacological characterization of the effects of 3,4-methylenedioxymethamphetamine ("ecstasy") and its enantiomers on lethality, core temperature, and locomotor activity in singly housed and crowded mice". Psychopharmacology (Berl) 166 (3): 202–211. March 2003. doi:10.1007/s00213-002-1261-5. PMID 12563544. 
  71. ↑ 71.0 71.1 71.2 71.3 Martinez-Price, Diana; Krebs-Thomson, Kirsten; Geyer, Mark (1 January 2002). "Behavioral Psychopharmacology of MDMA and MDMA-Like Drugs: A Review of Human and Animal Studies". Addiction Research & Theory (Informa UK Limited) 10 (1): 43–67. doi:10.1080/16066350290001704. ISSN 1606-6359. 
  72. ↑ 72.0 72.1 "A pharmacological analysis of mice with a targeted disruption of the serotonin transporter". Psychopharmacology (Berl) 195 (2): 147–166. December 2007. doi:10.1007/s00213-007-0910-0. PMID 17712549. 
  73. ↑ 73.0 73.1 "Serotonin 5-HT2B receptors are required for 3,4-methylenedioxymethamphetamine-induced hyperlocomotion and 5-HT release in vivo and in vitro". J Neurosci 28 (11): 2933–2940. March 2008. doi:10.1523/JNEUROSCI.5723-07.2008. PMID 18337424. 
  74. ↑ "Serotonin1B receptor activation mimics behavioral effects of presynaptic serotonin release". Neuropsychopharmacology 8 (3): 201–211. May 1993. doi:10.1038/npp.1993.22. PMID 8099482. 
  75. ↑ "Locomotor response to MDMA is attenuated in knockout mice lacking the 5-HT1B receptor". Psychopharmacology (Berl) 141 (2): 154–161. January 1999. doi:10.1007/s002130050819. PMID 9952039. 
  76. ↑ "Which neuroreceptors mediate the subjective effects of MDMA in humans? A summary of mechanistic studies". Hum Psychopharmacol 16 (8): 589–598. December 2001. doi:10.1002/hup.348. PMID 12404538. 
  77. ↑ 77.0 77.1 77.2 "Pharmacological studies of the acute effects of (+)-3,4-methylenedioxymethamphetamine on locomotor activity: role of 5-HT(1B/1D) and 5-HT(2) receptors". Neuropsychopharmacology 26 (1): 40–52. January 2002. doi:10.1016/S0893-133X(01)00345-1. PMID 11751031. 
  78. ↑ 78.0 78.1 78.2 78.3 78.4 "Locomotor stimulation produced by 3,4-methylenedioxymethamphetamine (MDMA) is correlated with dialysate levels of serotonin and dopamine in rat brain". Pharmacol Biochem Behav 90 (2): 208–217. August 2008. doi:10.1016/j.pbb.2008.02.018. PMID 18403002. 
  79. ↑ "3,4-N-methlenedioxymethamphetamine-induced hypophagia is maintained in 5-HT1B receptor knockout mice, but suppressed by the 5-HT2C receptor antagonist RS102221". Neuropsychopharmacology 30 (6): 1056–1063. June 2005. doi:10.1038/sj.npp.1300662. PMID 15668722. 
  80. ↑ "Role of 5-HT2A and 5-HT2C/B receptors in the acute effects of 3,4-methylenedioxymethamphetamine (MDMA) on striatal single-unit activity and locomotion in freely moving rats". Psychopharmacology (Berl) 181 (4): 676–687. October 2005. doi:10.1007/s00213-005-0038-z. PMID 16001122. 
  81. ↑ "Dopamine/Serotonin releasers as medications for stimulant addictions". Serotonin–Dopamine Interaction: Experimental Evidence and Therapeutic Relevance. Progress in Brain Research. 172. 2008. 385–406. doi:10.1016/S0079-6123(08)00919-9. ISBN 978-0-444-53235-0. 
  82. ↑ "Dual dopamine/serotonin releasers: potential treatment agents for stimulant addiction". Exp Clin Psychopharmacol 16 (6): 458–474. December 2008. doi:10.1037/a0014103. PMID 19086767. 
  83. ↑ "The serotonin 5-HT2C receptor and the non-addictive nature of classic hallucinogens". J Psychopharmacol 31 (1): 127–143. January 2017. doi:10.1177/0269881116677104. PMID 27903793. 
  84. ↑ "3,4-Methylenedioxymethamphetamine (MDMA) neurotoxicity in rats: a reappraisal of past and present findings". Psychopharmacology (Berl) 189 (4): 407–424. January 2007. doi:10.1007/s00213-006-0322-6. PMID 16541247. 
  85. ↑ 85.0 85.1 "Psychopharmacology and Neurotoxicology of Methamphetamine and 3,4-Methylenedioxymethamphetamine". Amphetamines: Neurobiological Mechanisms, Pharmacology and Effects. Hauppauge [NY]: Nova Biomedical Books. 2012. pp. 1–43. ISBN 978-1-61470-305-1. OCLC 726822553. https://psycnet.apa.org/record/2012-17476-001. 
  86. ↑ 86.0 86.1 86.2 "MDMA (3,4-Methylenedioxymethamphetamine) Analogues as Tools to Characterize MDMA-Like Effects: An Approach to Understand Entactogen Pharmacology". Curr Neuropharmacol 11 (5): 521–534. September 2013. doi:10.2174/1570159X11311050007. PMID 24403876. 
  87. ↑ "Alpha1-adrenergic receptors mediate the locomotor response to systemic administration of (+/-)-3,4-methylenedioxymethamphetamine (MDMA) in rats". Pharmacol Biochem Behav 86 (4): 622–630. April 2007. doi:10.1016/j.pbb.2007.02.006. PMID 17363047. 
  88. ↑ "Alpha-1 noradrenergic receptors contribute to psychostimulant-like effects of MDMA in humans (Poster 14)". CPDD 70th Annual Scientific Meeting, The Caribe Hilton, San Juan, Puerto Rico, June 14–19, 2008. June 2008. https://cpdd.org/Pages/Meetings/Meetings_PDFs/2008Programbook.pdf#page=81. 
  89. ↑ "3, 4-methylenedioxymethamphetamine (MDMA,'Ecstasy') and prazosin interactions in humans". 70th Annual Meeting of the College on Problems of Drug Dependence, San Juan, Puerto Rico. June 2008. https://scholar.google.com/scholar?cluster=14033061140609064122. 
  90. ↑ "α₁-Adrenergic receptors contribute to the acute effects of 3,4-methylenedioxymethamphetamine in humans". J Clin Psychopharmacol 33 (5): 658–666. October 2013. doi:10.1097/JCP.0b013e3182979d32. PMID 23857311. 
  91. ↑ "The norepinephrine transporter inhibitor reboxetine reduces stimulant effects of MDMA ("ecstasy") in humans". Clin Pharmacol Ther 90 (2): 246–255. August 2011. doi:10.1038/clpt.2011.78. PMID 21677639. 
  92. ↑ Kaur, Harpreet; Karabulut, Sedat; Gauld, James W.; Fagot, Stephen A.; Holloway, Kalee N.; Shaw, Hannah E.; Fantegrossi, William E. (1 September 2023). "Balancing Therapeutic Efficacy and Safety of MDMA and Novel MDXX Analogues as Novel Treatments for Autism Spectrum Disorder". Psychedelic Medicine 1 (3): 166–185. doi:10.1089/psymed.2023.0023. ISSN 2831-4425. PMID 40046567. "The role of DA in the abuse-related effects of psychostimulants is well established in animal models. Still, deletions of DA D1, D2, and D3 receptor genes in mice had minimal impact on MDMA-induced locomotor activity,97 and DAT inhibition did not affect neurocognitive effects of MDMA in cynomolgus monkeys.98 In humans, D2 receptor antagonists reduced amphetamine-induced and MDMA-induced euphoria only at doses that produced dysphoria on their own.99 Therefore, it seems likely that systems unrelated to DA may be principally responsible for the acute effects of MDMA.40". 
  93. ↑ "Differential contributions of dopamine D1, D2, and D3 receptors to MDMA-induced effects on locomotor behavior patterns in mice". Neuropsychopharmacology 31 (11): 2349–2358. November 2006. doi:10.1038/sj.npp.1301161. PMID 16855533. 
  94. ↑ 94.0 94.1 "Behavioral effects of the highly selective serotonin releasing agent 5-methoxy-6-methyl-2-aminoindan". Eur J Pharmacol 258 (1–2): 1–13. June 1994. doi:10.1016/0014-2999(94)90051-5. PMID 7925587. 
  95. ↑ "Substituted amphetamine derivatives. II. Behavioural effects in mice related to monoaminergic neurones". Acta Pharmacol Toxicol (Copenh) 41 (4): 353–368. October 1977. doi:10.1111/j.1600-0773.1977.tb02674.x. PMID 303437. 
  96. ↑ "3,4-Methylenedioxymethamphetamine (MDMA) as a unique model of serotonin receptor function and serotonin-dopamine interactions". J Pharmacol Exp Ther 297 (3): 846–852. June 2001. doi:10.1016/S0022-3565(24)29607-5. PMID 11356903. https://bibliography.maps.org/resource/983. 
  97. ↑ 97.0 97.1 97.2 97.3 97.4 97.5 97.6 "Therapeutic Potential of 5-HT2C Receptor Agonists for Addictive Disorders". ACS Chem Neurosci 6 (7): 1071–1088. July 2015. doi:10.1021/acschemneuro.5b00025. PMID 25870913. 
  98. ↑ "Anxiety-like effects induced by acute fluoxetine, sertraline or m-CPP treatment are reversed by pretreatment with the 5-HT2C receptor antagonist SB-242084 but not the 5-HT1A receptor antagonist WAY-100635". Int J Neuropsychopharmacol 4 (04): 399–408. December 2001. doi:10.1017/S1461145701002632. PMID 11806866. 
  99. ↑ "Chronic treatment with fluvoxamine desensitizes 5-HT2C receptor-mediated hypolocomotion in rats". Pharmacol Biochem Behav 78 (4): 683–689. August 2004. doi:10.1016/j.pbb.2004.05.003. PMID 15301922. 
  100. ↑ "[Effects of fluoxetine on locomotor activity: possible involvement of dopamine]" (in Russian). Zh Vyssh Nerv Deiat Im I P Pavlova 56 (4): 523–528. 2006. PMID 17025197. 
  101. ↑ "Sertraline and cocaine-induced locomotion in mice. I. Acute studies". Psychopharmacology (Berl) 103 (3): 297–305. 1991. doi:10.1007/BF02244282. PMID 2057535. 
  102. ↑ "Serotonin (5-HT) precursor loading with 5-hydroxy-l-tryptophan (5-HTP) reduces locomotor activation produced by (+)-amphetamine in the rat". Drug Alcohol Depend 114 (2–3): 147–152. April 2011. doi:10.1016/j.drugalcdep.2010.09.015. PMID 21071157. 
  103. ↑ 103.0 103.1 103.2 "5-HT(2A) and 5-HT(2C) receptors exert opposing effects on locomotor activity in mice". Neuropsychopharmacology 34 (8): 1958–1967. July 2009. doi:10.1038/npp.2009.29. PMID 19322172. 
  104. ↑ 104.0 104.1 104.2 "5-hydroxytryptamine 2C/1A receptors modulate the biphasic dose response of the head twitch response and locomotor activity induced by DOM in mice". Psychopharmacology (Berl) 241 (11): 2315–2330. November 2024. doi:10.1007/s00213-024-06635-4. PMID 38916640. 
  105. ↑ 105.0 105.1 105.2 105.3 105.4 105.5 105.6 105.7 "Effect of Hallucinogens on Unconditioned Behavior". Behavioral Neurobiology of Psychedelic Drugs. Current Topics in Behavioral Neurosciences. 36. 2018. pp. 159–199. doi:10.1007/7854_2016_466. ISBN 978-3-662-55878-2. 
  106. ↑ 106.0 106.1 106.2 Pharmacology and Toxicology of N-Benzylphenethylamine ("NBOMe") Hallucinogens. Current Topics in Behavioral Neurosciences. 32. 2017. pp. 283–311. doi:10.1007/7854_2016_64. ISBN 978-3-319-52442-9. 
  107. ↑ 107.0 107.1 "Locomotor and discriminative stimulus effects of four novel hallucinogens in rodents". Behav Pharmacol 28 (5): 375–385. August 2017. doi:10.1097/FBP.0000000000000309. PMID 28537942. 
  108. ↑ "The 5-hydroxytryptamine 2A receptor agonists DOI and 25CN-NBOH decrease marble burying and reverse 8-OH-DPAT-induced deficit in spontaneous alternation". Neuropharmacology 183. February 2021. doi:10.1016/j.neuropharm.2019.107838. PMID 31693871. 
  109. ↑ "The selective 5-HT2A receptor agonist 25CN-NBOH: Structure-activity relationship, in vivo pharmacology, and in vitro and ex vivo binding characteristics of [3H]25CN-NBOH". Biochem Pharmacol 177. July 2020. doi:10.1016/j.bcp.2020.113979. PMID 32298690. 
  110. ↑ "Tolerance and Tachyphylaxis to Head Twitches Induced by the 5-HT2A Agonist 25CN-NBOH in Mice". Front Pharmacol 9. 2018. doi:10.3389/fphar.2018.00017. PMID 29467649. 
  111. ↑ 111.0 111.1 111.2 111.3 "Therapeutic potential of 5-HT2C receptor ligands". ScientificWorldJournal 10: 1870–1885. September 2010. doi:10.1100/tsw.2010.180. PMID 20852829. 
  112. ↑ 112.0 112.1 "5-HT2C ligands: recent progress". Prog Med Chem. Progress in Medicinal Chemistry 46: 281–390. 2008. doi:10.1016/S0079-6468(07)00006-9. ISBN 978-0-444-53018-9. PMID 18381128. 
  113. ↑ 113.0 113.1 "Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential". Nat Commun 14 (1). December 2023. doi:10.1038/s41467-023-44016-1. PMID 38102107. 
  114. ↑ "The selective 5-HT2A receptor antagonist MDL 100,907 counteracts the psychomotor stimulation ensuing manipulations with monoaminergic, glutamatergic or muscarinic neurotransmission in the mouse--implications for psychosis". J Neural Transm Gen Sect 100 (3): 225–237. 1995. doi:10.1007/BF01276460. PMID 8748668. 
  115. ↑ "5-HT2 receptor antagonism reduces hyperactivity induced by amphetamine, cocaine, and MK-801 but not D1 agonist C-APB". Pharmacol Biochem Behav 63 (2): 237–243. June 1999. doi:10.1016/s0091-3057(98)00240-8. PMID 10371652. 
  116. ↑ 116.0 116.1 "Blockade of phencyclidine-induced hyperlocomotion by olanzapine, clozapine and serotonin receptor subtype selective antagonists in mice". Psychopharmacology (Berl) 129 (1): 79–84. January 1997. doi:10.1007/s002130050165. PMID 9122367. 
  117. ↑ "5-HT2A receptor antagonists block MK-801-induced stereotypy and hyperlocomotion". Eur J Pharmacol 358 (2): 111–116. October 1998. doi:10.1016/s0014-2999(98)00591-3. PMID 9808259. 
  118. ↑ "Antagonism of 5-hydroxytryptamine(2a) receptors attenuates the behavioral effects of cocaine in rats". J Pharmacol Exp Ther 297 (1): 357–363. April 2001. doi:10.1016/S0022-3565(24)29546-X. PMID 11259563. 
  119. ↑ "Involvement of serotonin in the modulation of cocaine-induced locomotor activity in the rat". Pharmacol Biochem Behav 59 (3): 595–611. March 1998. doi:10.1016/s0091-3057(97)00473-5. PMID 9512061. 
  120. ↑ "Trazodone: a novel, broad-spectrum antidepressant". Mod Probl Pharmacopsychiatry. Modern Trends in Pharmacopsychiatry 18: 49–69. 1982. doi:10.1159/000406236. ISBN 978-3-8055-3428-4. PMID 6124884. 
  121. ↑ "Trazodone (Desyrel, Mead-Johnson Pharmaceutical Division)". Drug Intell Clin Pharm 16 (1): 7–13. January 1982. doi:10.1177/106002808201600102. PMID 7032872. 
  122. ↑ "Trazodone--a new antidepressant". Life Sci 28 (22): 2449–2458. June 1981. doi:10.1016/0024-3205(81)90586-5. PMID 7019617. 
  123. ↑ "On the central antiserotonin action of trazodone". Pol J Pharmacol Pharm 31 (1): 25–33. 1979. PMID 482164. 
  124. ↑ "Clozapine-induced locomotor suppression is mediated by 5-HT2A receptors in the forebrain". Neuropsychopharmacology 37 (13): 2747–2755. December 2012. doi:10.1038/npp.2012.139. PMID 22871913. 
  125. ↑ "m-CPP hypolocomotion is selectively antagonized by compounds with high affinity for 5-HT(2C) receptors but not 5-HT(2A) or 5-HT(2B) receptors". Behav Pharmacol 12 (8): 613–620. December 2001. doi:10.1097/00008877-200112000-00005. PMID 11856898. 
  126. ↑ Cooper, Ignatius Alvarez; Beecher, Kate; Bartlett, Selena E.; Belmer, Arnauld (2021). "Role of the Serotonin 2B Receptor in the Reinforcing Effects of Psychostimulants". 5-HT2B Receptors. 35. Cham: Springer International Publishing. pp. 309–322. doi:10.1007/978-3-030-55920-5_18. ISBN 978-3-030-55919-9. 
  127. ↑ "Structure, Function, and Pharmaceutical Ligands of 5-Hydroxytryptamine 2B Receptor". Pharmaceuticals 14 (2): 76. January 2021. doi:10.3390/ph14020076. PMID 33498477. 
  128. ↑ "The central serotonin 2B receptor: a new pharmacological target to modulate the mesoaccumbens dopaminergic pathway activity". J Neurochem 114 (5): 1323–1332. September 2010. doi:10.1111/j.1471-4159.2010.06848.x. PMID 20534001. 
  129. ↑ "Central serotonin(2B) receptor blockade inhibits cocaine-induced hyperlocomotion independently of changes of subcortical dopamine outflow". Neuropharmacology 97: 329–337. October 2015. doi:10.1016/j.neuropharm.2015.06.012. PMID 26116760. 
  130. ↑ 130.0 130.1 "The serotonin 2C receptor antagonist SB 242084 exhibits abuse-related effects typical of stimulants in squirrel monkeys". The Journal of Pharmacology and Experimental Therapeutics 342 (3): 761–769. September 2012. doi:10.1124/jpet.112.195156. PMID 22685342. "There is also evidence to support our finding that administration of SB 242084 alone induces stimulant-like effects, because administration of a high dose of SB 242084 (1.0 mg/kg) significantly increased basal locomotor activity in rats (Zaniewska et al., 2009). [...] This discrepancy may be accounted for by highlighting the tested dose range within each experiment. For example, the dose of SB 242084 used for reinstatement experiments in the previous rodent study (0.5 mg/kg) also failed to induce significant locomotor effects (Fletcher et al., 2002). However, increasing the dose of SB 242084 to 1.0 mg/kg did produce a modest, but significant, effect on locomotor activity in a separate study (Zaniewska et al., 2009).". 
  131. ↑ "Interactions of serotonin (5-HT)2 receptor-targeting ligands and nicotine: locomotor activity studies in rats". Synapse 63 (8): 653–661. August 2009. doi:10.1002/syn.20645. PMID 19347958. 
  132. ↑ "Influence of the 5-HT(2C) receptor antagonist SB242,084 on behaviour produced by the 5-HT(2) agonist Ro60-0175 and the indirect 5-HT agonist dexfenfluramine". Br J Pharmacol 133 (4): 459–466. June 2001. doi:10.1038/sj.bjp.0704082. PMID 11399662. 
  133. ↑ "The effects of the 5-HT(2C) receptor antagonist SB242084 on locomotor activity induced by selective, or mixed, indirect serotonergic and dopaminergic agonists". Psychopharmacology (Berl) 187 (4): 515–525. September 2006. doi:10.1007/s00213-006-0453-9. PMID 16832658. 
  134. ↑ "Activation of mesolimbic dopamine function by phencyclidine is enhanced by 5-HT(2C/2B) receptor antagonists: neurochemical and behavioural studies". Neuropharmacology 39 (12): 2318–2328. September 2000. doi:10.1016/s0028-3908(00)00089-7. PMID 10974315. 
  135. ↑ "Understanding Central Nervous System Effects of Deliriant Hallucinogenic Drugs through Experimental Animal Models". ACS Chem Neurosci 10 (1): 143–154. January 2019. doi:10.1021/acschemneuro.8b00433. PMID 30252437. 
  136. ↑ "DARK Classics in Chemical Neuroscience: Atropine, Scopolamine, and Other Anticholinergic Deliriant Hallucinogens". ACS Chem Neurosci 10 (5): 2144–2159. May 2019. doi:10.1021/acschemneuro.8b00615. PMID 30566832. 
  137. ↑ 137.0 137.1 137.2 "Effects of Cannabidiol on Locomotor Activity". Life 12 (5): 652. April 2022. doi:10.3390/life12050652. PMID 35629320. Bibcode: 2022Life...12..652C. 
  138. ↑ "Opioid-induced rewards, locomotion, and dopamine activation: A proposed model for control by mesopontine and rostromedial tegmental neurons". Neurosci Biobehav Rev 83: 72–82. December 2017. doi:10.1016/j.neubiorev.2017.09.022. PMID 28951251. 
  139. ↑ "Opioid and nondopamine reward circuitry and state-dependent mechanisms". Ann N Y Acad Sci 1451 (1): 29–41. September 2019. doi:10.1111/nyas.13605. PMID 29512887. Bibcode: 2019NYASA1451...29F. 
  140. ↑ "Role of Efficacy as a Determinant of Locomotor Activation by Mu Opioid Receptor Ligands in Female and Male Mice". J Pharmacol Exp Ther 382 (1): 44–53. July 2022. doi:10.1124/jpet.121.001045. PMID 35489781. 
  141. ↑ "Targeting α1- and α2-adrenergic receptors as a countermeasure for fentanyl-induced locomotor and ventilatory depression". Environ Toxicol Pharmacol 110. September 2024. doi:10.1016/j.etap.2024.104527. PMID 39106924. 
  142. ↑ "Behavioral effects of delta-opioid receptor agonists: potential antidepressants?". Jpn J Pharmacol 90 (1): 1–6. September 2002. doi:10.1254/jjp.90.1. PMID 12396021. 
  143. ↑ "Delta Opioid Receptors and Modulation of Mood and Emotion". Delta Opioid Receptor Pharmacology and Therapeutic Applications. Handbook of Experimental Pharmacology. 247. 2018. pp. 179–197. doi:10.1007/164_2017_42. ISBN 978-3-319-95131-7. 
  144. ↑ "Trace Amines and Their Receptors". Pharmacol Rev 70 (3): 549–620. July 2018. doi:10.1124/pr.117.015305. PMID 29941461. 
  145. ↑ "In Vitro Characterization of Psychoactive Substances at Rat, Mouse, and Human Trace Amine-Associated Receptor 1". J Pharmacol Exp Ther 357 (1): 134–144. April 2016. doi:10.1124/jpet.115.229765. PMID 26791601. https://d1wqtxts1xzle7.cloudfront.net/74120533/eae6c6e62565b82d46b4d111bbea0f77b9c2-libre.pdf?1635931703=&response-content-disposition=inline%3B+filename%3DIn_Vitro_Characterization_of_Psychoactiv.pdf&Expires=1746838268&Signature=Sy4fJ90yUhxs68314NxYsW5PAaNrBGePRu35WRR4PIF-3YC7Z~sLdnCn5wfqqbLg9bDEGdt~oW55ugMP3D3jgA0BoRI~~GOb0NQOwrtfUEQK1PQs1uuN9qg5Y1ct8z5NsABm44RgtukkwRMdU6fO7OlfIsQ68hOiFk129Ll7UYqldxD2f1xhE2fTTfsxSpb8cMCJzHn7-ItqLdwnAUPFK7WggDIjmY1kCnaHLwIxMwdJCAq8L6DYzSTg7pZkbR8qlou~GXbTPQt~gYpyZTJp5hgW-7V6K5wLlQ7Z2xE7B0f9wEfuc1W1QNafg125Tr-vvAe4LEGKXV58bnn1bpfWKw__&Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA. 
  146. ↑ "Trace amine-associated receptor 1 modulates dopaminergic activity". J Pharmacol Exp Ther 324 (3): 948–956. March 2008. doi:10.1124/jpet.107.132647. PMID 18083911. 
  147. ↑ 147.0 147.1 147.2 147.3 "Trace amine-associated receptor 1 (TAAR1) agonism as a new treatment strategy for schizophrenia and related disorders". Trends Neurosci 46 (1): 60–74. January 2023. doi:10.1016/j.tins.2022.10.010. PMID 36369028. "In addition to enhanced dopamine release, TAAR1-KO mice show enhanced hyperlocomotion in response to psychostimulant drugs including amphetamine, methamphetamine, and 3,4-methylenedioxymethamphetamine (MDMA) [19,20,41,55], as well as to drugs that increase monoamine levels, such as MAO inhibitors [56]. By contrast, TAAR1-OE animals are hyposensitive to the stimulatory effects of amphetamine [54] in comparison to wild-type animals. [...] Three TAAR1 full agonists, RO5166017, RO5256390, and SEP-363856, were all able to prevent psychostimulant-induced hyperlocomotion in wild-type but not TAAR1-KO mice [47,78,79].". 
  148. ↑ "Genetic deletion of trace amine 1 receptors reveals their role in auto-inhibiting the actions of ecstasy (MDMA)". J Neurosci 31 (47): 16928–16940. November 2011. doi:10.1523/JNEUROSCI.2502-11.2011. PMID 22114263. 
  149. ↑ "The Trace Amine 1 receptor knockout mouse: an animal model with relevance to schizophrenia". Genes Brain Behav 6 (7): 628–639. October 2007. doi:10.1111/j.1601-183X.2006.00292.x. PMID 17212650. "Most notably, Caron & Gainetdinov (personal communication) have recently observed that group-housed TA1 KO mice show enhanced sensitivity to the locomotor stimulating effects of both amphetamine and b-PEA relative to group-housed WT littermates, as well as normal habituation to an open field.". 
  150. ↑ 150.0 150.1 "Trace Amines and the Trace Amine-Associated Receptor 1: Pharmacology, Neurochemistry, and Clinical Implications". Front Neurosci 10: 148. 2016. doi:10.3389/fnins.2016.00148. PMID 27092049. 
  151. ↑ 151.0 151.1 151.2 "Trace amine-associated receptor 1: A promising target for the treatment of psychostimulant addiction". Eur J Pharmacol 761: 345–352. August 2015. doi:10.1016/j.ejphar.2015.06.019. PMID 26092759. 
  152. ↑ 152.0 152.1 152.2 152.3 152.4 "Potential of Ligands for Trace Amine-Associated Receptor 1 (TAAR1) in the Management of Substance Use Disorders". CNS Drugs 35 (12): 1239–1248. December 2021. doi:10.1007/s40263-021-00871-4. PMID 34766253. 
  153. ↑ 153.0 153.1 153.2 "Brain-specific overexpression of trace amine-associated receptor 1 alters monoaminergic neurotransmission and decreases sensitivity to amphetamine". Neuropsychopharmacology 37 (12): 2580–2592. November 2012. doi:10.1038/npp.2012.109. PMID 22763617. 
  154. ↑ "Robust aversive effects of trace amine-associated receptor 1 activation in mice". Neuropsychopharmacology 48 (10): 1446–1454. September 2023. doi:10.1038/s41386-023-01578-4. PMID 37055488. 
  155. ↑ "Unlocking the Therapeutic Potential of Ulotaront as a Trace Amine-Associated Receptor 1 Agonist for Neuropsychiatric Disorders". Biomedicines 11 (7): 1977. July 2023. doi:10.3390/biomedicines11071977. PMID 37509616. 
  156. ↑ 156.0 156.1 "Discovery of Trace Amine Associated Receptor 1 (TAAR1) Agonist 2-(5-(4'-Chloro-[1,1'-biphenyl-4-yl)-4H-1,2,4-triazol-3-yl)ethan-1-amine (LK00764) for the Treatment of Psychotic Disorders"]. Biomolecules 12 (11). November 2022. doi:10.3390/biom12111650. PMID 36359001. 
  157. ↑ 157.0 157.1 "TAAR1 activation modulates monoaminergic neurotransmission, preventing hyperdopaminergic and hypoglutamatergic activity". Proc Natl Acad Sci U S A 108 (20): 8485–8490. May 2011. doi:10.1073/pnas.1103029108. PMID 21525407. Bibcode: 2011PNAS..108.8485R. 
  158. ↑ 158.0 158.1 "TAAR1 regulates drug-induced reinstatement of cocaine-seeking via negatively modulating CaMKIIα activity in the NAc". Mol Psychiatry 27 (4): 2136–2145. April 2022. doi:10.1038/s41380-022-01448-3. PMID 35079125. 
  159. ↑ 159.0 159.1 "Trace amine-associated receptor 1 partial agonism reveals novel paradigm for neuropsychiatric therapeutics". Biol Psychiatry 72 (11): 934–942. December 2012. doi:10.1016/j.biopsych.2012.05.014. PMID 22705041. "Psychostimulants like cocaine and d-amphetamine interact with the DA transporter (DAT) to elevate extracellular DA concentration. In rodents, this translates into excessive [locomotor activity (LMA)] (Figures 2A, B; Figure S3A, B in Supplement 1), the reversal of which can be used to predict the potential antipsychotic activity of drugs (22). RO5203648 given orally reduced hyperlocomotion in both rats and mice treated with cocaine (Figure 2A, B), although not at the highest dose in mice (10 mg/kg). RO5203648 reduced d-amphetamine-induced hyperlocomotion by one half at a high dose (30 mg/kg) in rats, whereas in mice it had no effect at the doses tested (Figure S3A, B in Supplement 1).". 
  160. ↑ "Effects of the trace amine-associated receptor 1 agonist RO5263397 on abuse-related effects of cocaine in rats". Neuropsychopharmacology 39 (10): 2309–2316. September 2014. doi:10.1038/npp.2014.91. PMID 24743376. 
  161. ↑ "Effects of the trace amine associated receptor 1 agonist RO5263397 on abuse-related behavioral indices of methamphetamine in rats". Int J Neuropsychopharmacol 18 (4). October 2014. doi:10.1093/ijnp/pyu060. PMID 25522401. 
  162. ↑ "Trace Amine-Associated Receptor 1 Agonists as Narcolepsy Therapeutics". Biol Psychiatry 82 (9): 623–633. November 2017. doi:10.1016/j.biopsych.2016.10.012. PMID 27919403. 
  163. ↑ "Trace amine-associated receptor 1 agonism promotes wakefulness without impairment of cognition in Cynomolgus macaques". Neuropsychopharmacology 44 (8): 1485–1493. July 2019. doi:10.1038/s41386-019-0386-8. PMID 30954024. 
  164. ↑ "Trace amine-associated receptor 1 modulates motor hyperactivity, cognition, and anxiety-like behavior in an animal model of ADHD". Prog Neuropsychopharmacol Biol Psychiatry 117. July 2022. doi:10.1016/j.pnpbp.2022.110555. PMID 35346791. 
  165. ↑ 165.0 165.1 "Therapeutic Potential of TAAR1 Agonists in Schizophrenia: Evidence from Preclinical Models and Clinical Studies". Int J Mol Sci 22 (24). December 2021. doi:10.3390/ijms222413185. PMID 34947997. 
  166. ↑ 166.0 166.1 "TAAR1 in Addiction: Looking Beyond the Tip of the Iceberg". Front Pharmacol 9. 2018. doi:10.3389/fphar.2018.00279. PMID 29636691. 
  167. ↑ 167.0 167.1 "A new perspective for schizophrenia: TAAR1 agonists reveal antipsychotic- and antidepressant-like activity, improve cognition and control body weight". Mol Psychiatry 18 (5): 543–556. May 2013. doi:10.1038/mp.2012.57. PMID 22641180. 
  168. ↑ "The trace amine-associated receptor 1 modulates methamphetamine's neurochemical and behavioral effects". Front Neurosci 9: 39. 2015. doi:10.3389/fnins.2015.00039. PMID 25762894. 
  169. ↑ "Towards Novel Treatments for Schizophrenia: Molecular and Behavioural Signatures of the Psychotropic Agent SEP-363856". Int J Mol Sci 22 (8): 4119. April 2021. doi:10.3390/ijms22084119. PMID 33923479. 
  170. ↑ ""TAARgeting Addiction"--The Alamo Bears Witness to Another Revolution: An Overview of the Plenary Symposium of the 2015 Behavior, Biology and Chemistry Conference". Drug Alcohol Depend 159: 9–16. February 2016. doi:10.1016/j.drugalcdep.2015.11.014. PMID 26644139. "[...] EPPTB's effect on the spontaneous locomotor activity in a familiar environment displayed by WT and taar1-deficient mice chronically exposed to 3 mg/kg METH (i.p.) over a range of doses was examined. The results of this study (Grandy, 2014; SfN abstracts) support the interpretation that EPPTB prevents to a significant degree METH-stimulated locomotor activity but only in WT mice with a history of chronic METH exposure.". 
  171. ↑ "A G protein-coupled receptor mechanism of action distinguishes methamphetamine from cocaine". Neuroscience 2014. 16 November 2014. https://www.abstractsonline.com/Plan/ViewAbstract.aspx?sKey=5a1aaa25-ae71-43f4-9d64-2dbe6fd43285&cKey=1800b5d6-aafa-471d-9209-7ff2f00ab8c6&mKey=54c85d94-6d69-4b09-afaa-502c0e680ca7. Retrieved 6 January 2025. "The TAAR1-selective antagonist EPPTB blocked methamphetamine- and bupropion-stimulated chloride conductance in Xenopous oocytes co-expressing mouse TAAR1 and the human cystic fibrosis transmembrane conductance regulator in a concentration-dependent manner with IC50's of 2.3±0.3nM and 4.3±0.7nM, respectively. [...] EPPTB displayed no affinity for mouse biogenic amine transporters nor did it produce a significant phenotype in wildtype or taar1-/- mice. In contrast, at the highest dose tested (100 mg/kg, i.p.) EPPTB inhibited approximately 70% of methamphetamine-stimulated (3 mg/kg, i.p.) activity in wildtype mice while having no effect on similarly treated [TAAR1] knockout mice. Intraperitoneal co-administration of methamphetamine (3 mg/kg) and bupropion (50 mg/kg) to wildtype mice produced greater activity than either drug alone, an effect absent from [TAAR1] knockout mice. [...] The existence of a methamphetamine-activated G protein-coupled receptor that is also activated by bupropion [...]" 
  172. ↑ "SEP-363856, a Novel Psychotropic Agent with a Unique, Non-D2 Receptor Mechanism of Action". J Pharmacol Exp Ther 371 (1): 1–14. October 2019. doi:10.1124/jpet.119.260281. PMID 31371483. 
  173. ↑ "Behavioral consequences of antidepressant treatment in rodents". Neurosci Biobehav Rev 10 (2): 123–134. 1986. doi:10.1016/0149-7634(86)90023-0. PMID 3526203. 
  174. ↑ "Neuropharmacology of light-induced locomotor activation". Neuropharmacology 95: 243–251. August 2015. doi:10.1016/j.neuropharm.2015.03.023. PMID 25842246. "It was found that visual stimulation of rats with white-light of 82 lux intensity induced locomotor activity and increased extracellular 5-HT and dopamine (DA) levels in the visual cortex (Müller et al., 2007a; Müller and Huston, 2007) and 5-HT in the medial prefrontal cortex (Pum et al., 2008). The 5-HT and DA increase were also seen in anesthetized animals (Pum et al., 2008). Cocaine, which induces serotonergic and dopaminergic activation (Izenwasser et al., 1990; Müller and Homberg, 2015), potentiates [light-induced locomotor activity (LIA)] (Pum et al., 2011).". 
  175. ↑ "Strategies for Behaviorally Phenotyping the Transgenic Mouse". Transgenic Mouse. Methods Mol Biol. 2066. 2020. pp. 171–194. doi:10.1007/978-1-4939-9837-1_15. ISBN 978-1-4939-9836-4. 



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