عامل إطلاق مونوامين
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↑  Reese EA، Bunzow JR، Arttamangkul S، Sonders MS، Grandy DK (أبريل 2007). "Trace amine-associated receptor 1 displays species-dependent stereoselectivity for isomers of methamphetamine, amphetamine, and para-hydroxyamphetamine". J Pharmacol Exp Ther. ج. 321 ع. 1: 178–186. DOI:10.1124/jpet.106.115402. PMID:17218486. مؤرشف من الأصل في 2025-01-20. اطلع عليه بتاريخ 2025-01-19. The EC50 of (+)-AMPH to release DA via DAT is 25 nM, with Ki uptake values in rat synaptosomes for this neurotransmitter of 34 nM at the DAT, concentrations approximately 20- to 30-fold lower than the EC50 values we calculated for eliciting an in vitro functional response from rTAAR1 (0.8 μM). Chronic METH abusers can typically consume gram quantities of drug per day (Kramer et al., 1967). [...] plasma concentrations of both drugs can reach into the high-micromolar range (Drummer and Odell, 2001; Baselt, 2002; Peters et al., 2003). Although the extracellular free concentration of METH around relevant human dopaminergic synapses presumably involved in producing desirable CNS effects is not known with certainty, in rats METH serum levels are typically 1/10 what is found in brain (Riviere et al., 2000). Forensic evidence indicates that experienced METH users can typically achieve peak blood concentrations of 100 μM (Baselt, 2002; Peters et al., 2003). Both isomers of METH were full agonists of h-rChTAAR1 over a range of EC50 values from 3.5 to ~15 μM, concentrations often exceeded in the blood of human METH addicts (Derlet et al., 1989). If TAAR1s, whether expressed in the CNS or periphery, are exposed to such concentrations, it is possible they could become functionally activated. [...] Given that the EC50 values for METH and AMPH activation of the h-rChTAAR1 in vitro are well below the concentrations frequently found in addicts, we suggest that TAAR1 might be a potential mediator of some of the effects of AMPH and METH in humans, including hyperthermia and stroke.
1 2  Espinoza S، Gainetdinov RR (2014). "Neuronal Functions and Emerging Pharmacology of TAAR1". Taste and Smell. Topics in Medicinal Chemistry. Cham: Springer International Publishing. ج. 23. ص. 175–194. DOI:10.1007/7355_2014_78. ISBN:978-3-319-48925-4. اطلع عليه بتاريخ 2025-01-19. Interestingly, the concentrations of amphetamine found to be necessary to activate TAAR1 are in line with what was found in drug abusers [3, 51, 52]. Thus, it is likely that some of the effects produced by amphetamines could be mediated by TAAR1. Indeed, in a study in mice, MDMA effects were found to be mediated in part by TAAR1, in a sense that MDMA auto-inhibits its neurochemical and functional actions [46]. Based on this and other studies (see other section), it has been suggested that TAAR1 could play a role in reward mechanisms and that amphetamine activity on TAAR1 counteracts their known behavioral and neurochemical effects mediated via dopamine neurotransmission.
↑  Grandy DK، Miller GM، Li JX (فبراير 2016). ""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. ج. 159: 9–16. DOI:10.1016/j.drugalcdep.2015.11.014. PMC:4724540. PMID:26644139. مؤرشف من الأصل في 2025-01-20. اطلع عليه بتاريخ 2025-01-19. That TAAR1 signaling is coupled to the inhibition of VTA DA neuron firing was a surprising finding. [...] earlier data suggested that TAAR1 activation leads to inhibition of DA uptake by DAT, promotion of DA efflux by DAT and DAT internalization which presumably would augment extracellular DA levels, whereas inhibition of DA neuronal firing rate would likely decrease extracellular DA levels, [...] this mismatch in expectations immediately attracted the attention of those trying to determine whether TAAR1 is a METH/AMPH and DA receptor in vivo as it is in vitro (Bunzow et al., 2001; Wainscott et al., 2007; Xie and Miller, 2009; Panas et al., 2012).
1 2 3  Dunlap LE، Andrews AM، Olson DE (أكتوبر 2018). "Dark Classics in Chemical Neuroscience: 3,4-Methylenedioxymethamphetamine" (PDF). ACS Chem Neurosci. ج. 9 ع. 10: 2408–2427. DOI:10.1021/acschemneuro.8b00155. PMC:6197894. PMID:30001118. مؤرشف من الأصل (pdf) في 2024-12-11. اطلع عليه بتاريخ 2025-01-19. [...] it is unclear if TAAR1 plays any role in the effects of MDMA in humans, as MDMA does not activate human TAAR1 in cellular assays like it does mouse and rat TAAR1.84
↑  Liu J، Wu R، Li JX (مارس 2020). "TAAR1 and Psychostimulant Addiction". Cellular and Molecular Neurobiology. ج. 40 ع. 2: 229–238. DOI:10.1007/s10571-020-00792-8. PMC:7845786. PMID:31974906. اطلع عليه بتاريخ 2025-01-19. Beside the TAAR1-KO mice, animals that overexpress taar1 in the brain were also generated, which was named as taar1 Tg mice (Revel et al. 2012a). Before discussing the behaviors of this line of taar1 Tg mice, it should be kept in mind that taar1 was expressed in all types of neurons in the whole brain of this mice strain, which is in contrast with the specifc expression pattern of that in the wildtype animals (Revel et al. 2012a). The electrophysiological results showed that excitatory and inhibitory inputs into the VTA were altered in the taar1 Tg mice (Revel et al. 2012a). Interestingly, although the basal levels of dopamine and norepinephrine in the nucleus accumbens (NAc) were elevated, amphetamine did not alter dopamine levels in the taar1 Tg mice (Revel et al. 2012a). Consistently, behavioral test showed that AMPH led to hyperactivity in WT but not in taar1 Tg mice (Revel et al. 2012a).
1 2 3 4 5 6  Small C، Cheng MH، Belay SS، Bulloch SL، Zimmerman B، Sorkin A، Block ER (أغسطس 2023). "The Alkylamine Stimulant 1,3-Dimethylamylamine Exhibits Substrate-Like Regulation of Dopamine Transporter Function and Localization". J Pharmacol Exp Ther. ج. 386 ع. 2: 266–273. DOI:10.1124/jpet.122.001573. PMC:10353075. PMID:37348963. مؤرشف من الأصل في 2025-01-20. اطلع عليه بتاريخ 2025-01-19. [...] a proposed intracellular target for amphetamine is the [TAAR1], a [GPCR] that is expressed on intracellular membranes in DA neurons (Miller, 2011). Phenethylamine stimulants have been proposed to activate TAAR1, leading to increased cAMP generation and RhoA activation, with subsequent enhancement of DAT reverse transport and endocytosis (Xie and Miller, 2007, 2008, 2009; Underhill et al., 2021). Methamphetamine-induced DAT endocytosis was found to be dependent on TAAR1 expression and PKA activity as suggested by use of the kinase inhibitor H89 (Xie and Miller, 2009). However, evidence indicating that amphetamine-induced endocytosis is independent of TAAR1 includes 1) HEK-293 cells do not express TAAR1 (Reese et al., 2007; Xie and Miller, 2007) but do exhibit amphetamine-induced DAT endocytosis [present studies and (Saunders et al., 2014; Cheng et al., 2015; Wheeler et al., 2015)]؛ 2) cAMP and PKA activation, which are stimulated by TAAR1, antagonized amphetamine-induced DAT endocytosis in heterologous cells and DA neurons [present studies and (Wheeler et al., 2015)]؛ and 3) in cell lines and rodent striatal synaptosomes, PKA activation increased DAT Vmax, consistent with increased plasma membrane expression (Pristupa et al., 1998; Page et al., 2004; Batchelor and Schenk, 2018). Additionally, DMAA induced DAT endocytosis (Figs. 3 and 4) despite exhibiting no activity at human TAAR1 in receptor binding studies (Rickli et al., 2019). Therefore, although some evidence does support a role of TAAR1 in modulating amphetamine-induced DAT endocytosis, the present studies suggest that DMAA and amphetamine promote DAT endocytosis through a TAAR1-independent mechanism.
↑  Xu Z، Li Q (مارس 2020). "TAAR Agonists". Cell Mol Neurobiol. ج. 40 ع. 2: 257–272. DOI:10.1007/s10571-019-00774-5. PMID:31848873. اطلع عليه بتاريخ 2025-01-19. Amphetamine might act on TAAR1 to activate Gαs pathway and phosphorylate monoamine transporter such as dopamine transporter (DAT), leading to its internalization and ceased transport (Bunzow et al. 2001; Miller 2011). Behaviorally, knockout of TAAR1 in mice leads to locomotor supersensitivity induced by amphetamine, although the connection to regulation of monoamine system is undetermined and needs further investigation (Achat-Mendes et al. 2012; Lindemann et al. 2008).
↑  Reese، Edmund Arthur (2008). Trace amine-associated receptor 1 : a novel target of methamphetamine. World Development (Thesis). DOI:10.6083/M4ZK5DNR. مؤرشف من الأصل في 2020-02-18. اطلع عليه بتاريخ 2025-01-19. In a recent study it was reported that AMPH induced locomotor function of TAAR1 knockout mice was increased compared to the response of wild type mice (Lindemann et al., 2007). In addition, they reported a 2½ fold increase in dopamine, noradrenaline, and serotonin release, in response to AMPH, in TAAR1 knockout mice compared to wild type mice. These results are similar to the increase in DA and NE release reported in a study of another TAAR1 KO mouse (Wolinsky et al., 2007). These findings of increased DA release and increased locomoter effects in the TAAR1 KO are reconciled with the proposed model as follows. The increased DA release of the TAAR1 KO may be due to reduced DAT internalization. With more DAT (or NET or SERT) remaining at the cell surface, more neurotransmitters can be reverse exchanged upon application of AMPH. The increased DA release would also explain the increased locomotor activity of the KO vs WT. The WT TAAR1 cells would undergo DAT internalization as described in the model. With fewer surface transporters, less DA would be reverse exchanged resulting in less DA release compared to levels in the KO mice.
↑  Wu R، Li JX (ديسمبر 2021). "Potential of Ligands for Trace Amine-Associated Receptor 1 (TAAR1) in the Management of Substance Use Disorders". CNS Drugs. ج. 35 ع. 12: 1239–1248. DOI:10.1007/s40263-021-00871-4. PMC:8787759. PMID:34766253. اطلع عليه بتاريخ 2025-01-19. Moreover, while deletion of TAAR1 led to increased frequency of spontaneous firing frequency of serotonin neurons in brain slices [36], TAAR1 full agonists significantly inhibited the firing frequency in DRN serotonin neurons [28, 38]. [...] In vitro electrophysiological recordings showed a remarkable increase in the spontaneous firing rate of dopamine neurons in the VTA of TAAR1-KO mice [36]. While the endogenous TAAR1 agonist TYR decreased the firing rate of dopamine neurons in slices from WT mice, it had no effect in slices from TAAR1-KO mice [36]. [...] Similar to TYR, [the TAAR1 full agonist] RO5166017 reduced the firing rate of VTA dopamine neurons and DRN serotonin neurons in brain slices from WT but not TAAR1-KO mice, through the activation of K+-mediated outward current, which can be blocked by TAAR1 antagonist EPPTB [38]. [...] [The TAAR1 full agonist] RO5256390 decreased the firing frequency of VTA dopamine and DRN serotonin neurons in brain slices from WT but not TAAR1-KO mice, [...]
↑  Simmler LD، Buser TA، Donzelli M، Schramm Y، Dieu LH، Huwyler J، Chaboz S، Hoener MC، Liechti ME (يناير 2013). "Pharmacological characterization of designer cathinones in vitro". Br J Pharmacol. ج. 168 ع. 2: 458–470. DOI:10.1111/j.1476-5381.2012.02145.x. PMC:3572571. PMID:22897747. مؤرشف من الأصل في 2025-01-09. اطلع عليه بتاريخ 2025-01-19. β-Keto-analogue cathinones also exhibited approximately 10-fold lower affinity for the TA1 receptor compared with their respective non-β-keto amphetamines. [...] Activation of TA1 receptors negatively modulates dopaminergic neurotransmission. Importantly, methamphetamine decreased DAT surface expression via a TA1 receptor-mediated mechanism and thereby reduced the presence of its own pharmacological target (Xie and Miller, 2009). MDMA and amphetamine have been shown to produce enhanced DA and 5-HT release and locomotor activity in TA1 receptor knockout mice compared with wild-type mice (Lindemann et al., 2008; Di Cara et al., 2011). Because methamphetamine and MDMA auto-inhibit their neurochemical and functional effects via TA1 receptors, low affinity for these receptors may result in stronger effects on monoamine systems by cathinones compared with the classic amphetamines.
1 2 3  Daberkow DP، Brown HD، Bunner KD، Kraniotis SA، Doellman MA، Ragozzino ME، Garris PA، Roitman MF (يناير 2013). "Amphetamine paradoxically augments exocytotic dopamine release and phasic dopamine signals". J Neurosci. ج. 33 ع. 2: 452–463. DOI:10.1523/JNEUROSCI.2136-12.2013. PMC:3711765. PMID:23303926. اطلع عليه بتاريخ 2025-01-19. Drugs of abuse hijack brain-reward circuitry during the addiction process by augmenting action potential-dependent phasic dopamine release events associated with learning and goal-directed behavior. One prominent exception to this notion would appear to be amphetamine (AMPH) and related analogs, which are proposed instead to disrupt normal patterns of dopamine neurotransmission by depleting vesicular stores and promoting nonexocytotic dopamine efflux via reverse transport. This mechanism of AMPH action, though, is inconsistent with its therapeutic effects and addictive properties, which are thought to be reliant on phasic dopamine signaling. [...] These findings identify upregulation of exocytotic dopamine release as a key AMPH action in behaving animals and support a unified mechanism of abused drugs to activate phasic dopamine signaling. [...] Our results also raise the possibility that enhanced phasic dopamine signaling may underlie important clinical effects of AMPH. Modest activation of dopamine transients at the relatively low dose of 1 mg/kg used here may be an important action of medications that combine amphetamine salts (e.g., Adderall) used clinically (Joyce et al., 2007). Indeed, low doses of AMPH preserve and improve learning and behavioral performance (Mayorga et al., 2000; Wyvell and Berridge, 2000; Taylor and Jentsch, 2001; Zhang et al., 2003; Knutson et al., 2004). In contrast, high doses of AMPH can produce a behavioral profile similar to the positive symptoms associated with schizophrenia (Featherstone et al., 2007; Lisman et al., 2008). [...] Thus, disrupting the tight temporal concurrence between dopamine transients and important external cues due to hyperactive phasic dopamine signaling may contribute to AMPH-induced psychosis (Featherstone et al., 2007).
1 2 3  Covey DP، Juliano SA، Garris PA (2013). "Amphetamine elicits opposing actions on readily releasable and reserve pools for dopamine". PLOS ONE. ج. 8 ع. 5: e60763. Bibcode:2013PLoSO...860763C. DOI:10.1371/journal.pone.0060763. PMC:3643976. PMID:23671560. اطلع عليه بتاريخ 2025-01-19. While there is little debate that behavioral effects of this important psychostimulant are associated with a hyperdopamine state [3–6], the underlying mechanisms by which this condition manifests have been the subject of intense study. Two, what ostensibly appear to be mutually exclusive, views have emerged. On the one hand, AMPH enhances tonic dopamine signaling by reversing dopamine transporter (DAT) direction, leading to a non-exocytotic, action potential-independent type of release or efflux that is driven by vesicular depletion and the redistribution of dopamine to the cytosol [7,8]. On the other hand, AMPH enhances phasic dopamine signaling by promoting burst firing of dopamine neurons [9,10], inhibiting dopamine uptake [11,12], and upregulating vesicular dopamine release [13,14]. How AMPH concurrently activates tonic and phasic dopamine signaling, the two fundamental modes of communication used by dopamine neurons [15], yet elicits opposing actions on vesicular dopamine stores is perplexing and unresolved.
↑  Higgins GA، Fletcher PJ (يوليو 2015). "Therapeutic Potential of 5-HT2C Receptor Agonists for Addictive Disorders". ACS Chem Neurosci. ج. 6 ع. 7: 1071–1088. DOI:10.1021/acschemneuro.5b00025. PMID:25870913. مؤرشف من الأصل في 2023-05-15. اطلع عليه بتاريخ 2025-01-19. The sampling of extracellular fluids using in vivo microdialysis provides a direct way to study drug effects on synaptic efflux of a neurotransmitter. Comparisons of dexfenfluramine and fluoxetine using this technique have revealed a significant difference between the effects of reuptake inhibition and release on extracellular 5-HT levels.34−36 For example, Tao et al.35 compared the effects of fluoxetine and dexfenfluramine on extracellular 5-HT in the hypothalamus, with the latter increasing basal 5-HT 6−16-fold, compared to 3-fold following fluoxetine (Figure 1A). These differences in magnitude reflect differences in the way that fluoxetine and dexfenfluramine elevate 5-HT. The ability of SSRIs to increase extracellular 5- HT is dependent on neuronal activity (i.e., impulse dependent) and is subject to autoreceptor feedback inhibition. In contrast, (dex)fenfluramine increases extracellular 5-HT by disrupting vesicular storage and promoting nonexocytotic release that is independent of both of these regulatory factors.36 [...] Figure 1. Comparison between a 5-HT releaser (dexfenfluramine) and SSRI (fluoxetine) on (A) extracellular 5-HT release sampled from rat hypothalamus, [...]
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↑  Cheetham SC، Kulkarni RS، Rowley HL، Heal DJ (2007). "The SH rat model of ADHD has profoundly different catecholaminergic responses to amphetamine's enantiomers compared with Sprague-Dawleys". Neuroscience 2007, San Diego, CA, Nov 3-7, 2007. https://www.abstractsonline.com/pp8/#!/1820. Society for Neuroscience. مؤرشف من الأصل في 2024-07-27. اطلع عليه بتاريخ 2025-01-19. Both d- and l-[amphetamine (AMP)] evoked rapid increases in extraneuronal concentrations of [noradrenaline (NA)] and [dopamine (DA)] that reached a maximum 30 or 60 min after administration. However, the [spontaneously hypertensive rats (SHRs)] were much more responsive to AMP's enantiomers than the [Sprague-Dawleys (SDs)]. Thus, 3 mg/kg d-AMP produced a peak increase in [prefrontal cortex (PFC)] NA of 649 ± 87% (p<0.001) in SHRs compared with 198 ± 39% (p<0.05) in SDs; the corresponding figures for [striatal (STR)] DA were 4898 ± 1912% (p<0.001) versus 1606 ± 391% (p<0.001). At 9 mg/kg, l-AMP maximally increased NA efflux by 1069 ± 105% (p<0.001) in SHRs compared with 157 ± 24% (p<0.01) in SDs; the DA figures were 3294 ± 691% (p<0.001) versus 459 ± 107% (p<0.001). {{استشهاد بمنشورات مؤتمر}}: |مسار المؤتمر= بحاجة لعنوان (مساعدة)
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1 2  Underhill SM، Hullihen PD، Chen J، Fenollar-Ferrer C، Rizzo MA، Ingram SL، Amara SG (أبريل 2021). "Amphetamines signal through intracellular TAAR1 receptors coupled to Gα13 and GαS in discrete subcellular domains". Mol Psychiatry. ج. 26 ع. 4: 1208–1223. DOI:10.1038/s41380-019-0469-2. PMC:7038576. PMID:31399635. مؤرشف من الأصل في 2024-12-14. اطلع عليه بتاريخ 2025-01-19. Although the precise physiological role of TAAR1/G13-mediated DAT internalization remains to be established, it is likely that this pathway evolved to regulate the actions of endogenous amines including β-PEA, tyramine, 3-methoxytyramine, and DA. DA is a TAAR1 agonist (Fig. 1c) and recently, it was shown that the sustained elevation of extracellular DA seen following burst firing appears to be a consequence of DAT internalization by a Rho-dependent mechanism [51]. These results provide the first evidence that dopamine itself can act as a TAAR1 agonist to trigger transporter internalization in vivo. TAAR1 signaling also has the potential to serve as a sensor of cytoplasmic DA and its metabolites. At high cytosolic concentrations, DA becomes neurotoxic due to the formation of reactive oxygen species and quinones that can cause damage to the neuron [52]. Under normal conditions, DA transported through the DAT from the extracellular space is rapidly repackaged into synaptic vesicles or enzymatically metabolized. However, if cytoplasmic DA concentrations saturate these mechanisms, the reduction in surface levels of DAT mediated by TAAR1/G13 signaling may provide an additional means for maintaining free cytosolic DA below toxic levels.
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↑  Angoa-Pérez M، Anneken JH، Kuhn DM (2017). "Neurotoxicology of Synthetic Cathinone Analogs". Curr Top Behav Neurosci. Current Topics in Behavioral Neurosciences. ج. 32: 209–230. DOI:10.1007/7854_2016_21. ISBN:978-3-319-52442-9. PMC:6100737. PMID:27753008. اطلع عليه بتاريخ 2025-01-19. This flooding of the cytoplasm and synaptic space with the oxidatively labile DA is thought to be a critical first step in the neurotoxic cascade of the amphetamines [73]. These conditions of elevated concentrations of cytosolic monoamines could be further aggravated by inhibition of MAO [91]. Unlike amphetamines, mephedrone and methylone have little if any affinity for VMAT-2 [33]. Therefore, their lack of neurotoxicity could derive from an inability to promote the release of DA from storage vesicles into the cytoplasm.
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