عامل إطلاق مونوامين
مراجع

1 2 3  Baumeister AA (2021). "Is Attention-Deficit/Hyperactivity Disorder a Risk Syndrome for Parkinson's Disease?" (PDF). Harv Rev Psychiatry. ج. 29 ع. 2: 142–158. DOI:10.1097/HRP.0000000000000283. PMID:33560690. مؤرشف من الأصل (pdf) في 2024-09-03. اطلع عليه بتاريخ 2025-01-19. It has been suggested that the association between PD and ADHD may be explained, in part, by toxic effects of these drugs on DA neurons.241 [...] An important question is whether amphetamines, as they are used clinically to treat ADHD, are toxic to DA neurons. In most of the animal and human studies cited above, stimulant exposure levels are high relative to clinical doses, and dosing regimens (as stimulants) rarely mimic the manner in which these drugs are used clinically. The study by Ricaurte and colleagues248 is an exception. In that study, baboons orally self-administered a racemic (3:1 d/l) amphetamine mixture twice daily in increasing doses ranging from 2.5 to 20 mg/day for four weeks. Plasma amphetamine concentrations, measured at one-week intervals, were comparable to those observed in children taking amphetamine for ADHD. Two to four weeks after cessation of amphetamine treatment, multiple markers of striatal DA function were decreased, including DA and DAT. In another group of animals (squirrel monkeys), d/l amphetamine blood concentration was titrated to clinically comparable levels for four weeks by administering varying doses of amphetamine by orogastric gavage. These animals also had decreased markers of striatal DA function assessed two weeks after cessation of amphetamine.
↑  Asser A، Taba P (2015). "Psychostimulants and movement disorders". Front Neurol. ج. 6: 75. DOI:10.3389/fneur.2015.00075. PMC:4403511. PMID:25941511. اطلع عليه بتاريخ 2025-01-19. Amphetamine treatment similar to that used for ADHD has been demonstrated to produce brain dopaminergic neurotoxicity in primates, causing the damage of dopaminergic nerve endings in the striatum that may also occur in other disorders with long-term amphetamine treatment (57).
1 2  Advokat C (يوليو 2007). "Update on amphetamine neurotoxicity and its relevance to the treatment of ADHD". J Atten Disord. ج. 11 ع. 1: 8–16. DOI:10.1177/1087054706295605. PMID:17606768. مؤرشف من الأصل في 2022-10-24. اطلع عليه بتاريخ 2025-01-19.
↑  Berman SM، Kuczenski R، McCracken JT، London ED (فبراير 2009). "Potential adverse effects of amphetamine treatment on brain and behavior: a review". Mol Psychiatry. ج. 14 ع. 2: 123–142. DOI:10.1038/mp.2008.90. PMC:2670101. PMID:18698321. مؤرشف من الأصل في 2024-12-20. اطلع عليه بتاريخ 2025-01-19. Though the paradigm used by Ricaurte et al. 53 arguably still incorporates amphetamine exposure at a level above much clinical use,14,55 it raises important unanswered questions. Is there a threshold of amphetamine exposure above which persistent changes in the dopamine system are induced? [...]
↑  Ricaurte GA، Mechan AO، Yuan J، Hatzidimitriou G، Xie T، Mayne AH، McCann UD (أكتوبر 2005). "Amphetamine treatment similar to that used in the treatment of adult attention-deficit/hyperactivity disorder damages dopaminergic nerve endings in the striatum of adult nonhuman primates". J Pharmacol Exp Ther. ج. 315 ع. 1: 91–98. DOI:10.1124/jpet.105.087916. PMID:16014752. مؤرشف من الأصل في 2025-01-20. اطلع عليه بتاريخ 2025-01-19.
↑  Courtney KE، Ray LA (2016). "Clinical neuroscience of amphetamine-type stimulants: From basic science to treatment development". Prog Brain Res. ج. 223: 295–310. DOI:10.1016/bs.pbr.2015.07.010. PMID:26806782. مؤرشف من الأصل في 2024-08-14. اطلع عليه بتاريخ 2025-01-19. Repeated exposure to moderate to high levels of methamphetamine has been related to neurotoxic effects on the dopaminergic and serotonergic systems, leading to potentially irreversible loss of nerve terminals and/or neuron cell bodies (Cho and Melega, 2002). Preclinical evidence suggests that d-amphetamine, even when administered at commonly prescribed therapeutic doses, also results in toxicity to brain dopaminergic axon terminals (Ricaurte et al., 2005).
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1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21  Nagai F، Nonaka R، Satoh Hisashi Kamimura K (مارس 2007). "The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain". European Journal of Pharmacology. ج. 559 ع. 2–3: 132–137. DOI:10.1016/j.ejphar.2006.11.075. PMID:17223101. اطلع عليه بتاريخ 2025-01-19.
1 2 3 4 5 6  Del Bello F، Sakloth F، Partilla JS، Baumann MH، Glennon RA (سبتمبر 2015). "Ethylenedioxy homologs of N-methyl-(3,4-methylenedioxyphenyl)-2-aminopropane (MDMA) and its corresponding cathinone analog methylenedioxymethcathinone: Interactions with transporters for serotonin, dopamine, and norepinephrine". Bioorg Med Chem. ج. 23 ع. 17: 5574–5579. DOI:10.1016/j.bmc.2015.07.035. PMC:4562428. PMID:26233799. The present findings with MDMA are consistent with our previous data [15,17] and those reported by Simmler et al. [4] and Eshleman et al. [23] who examined the effects of MDMA and related drugs in human embryonic kidney (HEK) cells transfected with human SERT, DAT and NET. Thus, the molecular mechanism of action for MDMA at monoamine transporters is similar in rats and humans. On the other hand, the potency of (±)MDMA for releasing monoamines in rat brain synaptosomes shown here (i.e., 60–70 nM) is greater than its potency in transfected HEK cells (i.e., 1–20 μM). Such discrepancies in absolute potency could be related to species differences in drug responsiveness, differences in release assay methods employed, or the absence of important neuronal membrane proteins in non-neuronal HEK cells.
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↑  Schlessinger A، Geier E، Fan H، Irwin JJ، Shoichet BK، Giacomini KM، Sali A (سبتمبر 2011). "Structure-based discovery of prescription drugs that interact with the norepinephrine transporter, NET". Proc Natl Acad Sci U S A. ج. 108 ع. 38: 15810–15815. Bibcode:2011PNAS..10815810S. DOI:10.1073/pnas.1106030108. PMC:3179104. PMID:21885739. مؤرشف من الأصل في 2023-06-24. اطلع عليه بتاريخ 2025-01-19.
1 2 3 4  Partilla، John S.؛ Baumann، Michael H.؛ Decker، Ann M.؛ Blough، Bruce E.؛ Rothman، Richard B. (2016). "Interrogating the Activity of Ligands at Monoamine Transporters in Rat Brain Synaptosomes". Neurotransmitter Transporters. New York, NY: Springer New York. ج. 118. ص. 41–52. DOI:10.1007/978-1-4939-3765-3_3. ISBN:978-1-4939-3763-9. اطلع عليه بتاريخ 2025-01-19.
↑  Rothman RB، Dersch CM، Baumann MH، Carroll FI، Partilla JS (1999). "Development of a High-Throughput Assay for Biogenic Amine Transporter Substrates". Problems of Drug Dependence 1999: Proceedings of the 61st Annual Scientific Meeting, The College on Problems of Drug Dependence, Inc (PDF). NIDA Res Monogr. ج. 180. ص. 1–476 (251). PMID:11680410. مؤرشف من الأصل (PDF) في 2024-11-28. اطلع عليه بتاريخ 2025-01-19. The major goal of this study was to establish a high-throughput assay to detect [monoamine transporter substrates (SBSTs)] for use in a project to develop new drugs with dual activity as SBSTs of DAT and SERT. METHODS. Using minor modifications of published procedures, rat brain synaptosomes were preloaded with either [3H]DA, [3H]NE or [3H]5-HT. Test drugs were added and the reaction terminated by rapid filtration over Whatman GF/B filters. Release was quantified by counting how much tritium was retained on the filters. RESULTS. Using optimized conditions known SBSTs potently decreased retained tritium in a dose-dependent manner whereas known [uptake inhibitors (UIs)] were weak or ineffective. UIs shifted SBST inhibition curves to the right, consistent with antagonist-like activity. CONCLUSION. We have developed high throughput assays which detect SBSTs for the DA, 5-HT and NE transporters.
1 2 3 4 5 6 7 8  Partilla JS، Dersch CM، Baumann MH، Carroll FI، Rothman RB (1999). "Profiling CNS Stimulants with a High-Throughput Assay for Biogenic Amine Transporter Substractes". Problems of Drug Dependence 1999: Proceedings of the 61st Annual Scientific Meeting, The College on Problems of Drug Dependence, Inc (PDF). NIDA Res Monogr. ج. 180. ص. 1–476 (252). PMID:11680410. مؤرشف من الأصل (PDF) في 2024-11-28. اطلع عليه بتاريخ 2025-01-19. RESULTS. Methamphetamine and amphetamine potently released NE (IC50s = 14.3 and 7.0 nM) and DA (IC50s = 40.4 nM and 24.8 nM), and were much less potent releasers of 5-HT (IC50s = 740 nM and 1765 nM). Phentermine released all three biogenic amines with an order of potency NE (IC50 = 28.8 nM)> DA (IC50 = 262 nM)> 5-HT (IC50 = 2575 nM). Aminorex released NE (IC50 = 26.4 nM), DA (IC50 = 44.8 nM) and 5-HT (IC50 = 193 nM). Chlorphentermine was a very potent 5-HT releaser (IC50 = 18.2 nM), a weaker DA releaser (IC50 = 935 nM) and inactive in the NE release assay. Chlorphentermine was a moderate potency inhibitor of [3H]NE uptake (Ki = 451 nM). Diethylpropion, which is self-administered, was a weak DA uptake inhibitor (Ki = 15 µM) and NE uptake inhibitor (Ki = 18.1 µM) and essentially inactive in the other assays. Phendimetrazine, which is self-administered, was a weak DA uptake inhibitor (IC50 = 19 µM), a weak NE uptake inhibitor (8.3 µM) and essentially inactive in the other assays.
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19  Blough BE، Landavazo A، Partilla JS، Baumann MH، Decker AM، Page KM، Rothman RB (يونيو 2014). "Hybrid dopamine uptake blocker-serotonin releaser ligands: a new twist on transporter-focused therapeutics". ACS Med Chem Lett. ج. 5 ع. 6: 623–627. DOI:10.1021/ml500113s. PMC:4060932. PMID:24944732. اطلع عليه بتاريخ 2025-01-19.
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1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16  Walther D، Shalabi AR، Baumann MH، Glennon RA (يناير 2019). "Systematic Structure-Activity Studies on Selected 2-, 3-, and 4-Monosubstituted Synthetic Methcathinone Analogs as Monoamine Transporter Releasing Agents". ACS Chem Neurosci. ج. 10 ع. 1: 740–745. DOI:10.1021/acschemneuro.8b00524. PMC:8269283. PMID:30354055. اطلع عليه بتاريخ 2025-01-19.
↑  Baggott M (21 يناير 2022). "[Comment]". Artificial Intelligence. اطلع عليه بتاريخ 2025-01-19. I measured DA and 5-HT release in vitro and [2-FMA] basically didn't release 5-HT (EC50s were around 90 nM at DAT and 15000 nM at SERT).
↑  Baggott M (30 أبريل 2024). "[Comment]". Artificial Intelligence. اطلع عليه بتاريخ 2025-01-19. [2-FMA is] a potent substrate-type releaser at NET and DAT (EC50s below 100 nM) but not SERT. [...] It's my own (Tactogen's, really) unpublished data. I assayed it while trying to understand the Borax combo.
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