Relevant bibliographies by topics / Monoamine transporter

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Monoamine transporter'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Monoamine transporter"

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Nishimura, Mitsuhiro, Kohji Sato, Tomoya Okada, et al. "Ketamine Inhibits Monoamine Transporters Expressed in Human Embryonic Kidney 293 Cells." Anesthesiology 88, no. 3 (1998): 768–74. http://dx.doi.org/10.1097/00000542-199803000-00029.

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Background Ketamine has been characterized as having psychotomimetic and sympathomimetic effects. These symptoms have raised the possibility that ketamine affects monoaminergic neurotransmission. To elucidate the relation between ketamine and monoamine transporters, the authors constructed three cell lines that stably express the norepinephrine, dopamine, and serotonin transporters and investigated the effects of ketamine on these transporters. Methods Human embryonic kidney cells were transfected using the Chen-Okayama method with the human norepinephrine, rat dopamine, and rat serotonin transporter cDNA subcloned into the eukaryotic expression vector. Using cells stably expressing these transporters, the authors investigated the effects of ketamine on the uptake of these compounds and compared them with those of pentobarbital. Results Inhibition analysis showed that ketamine significantly inhibited the uptake of all three monoamine transporters in a dose-dependent manner. The Ki (inhibition constant) values of ketamine on the norepinephrine, dopamine, and serotonin transporters were 66.8 microM, 62.9 microM, and 162 microM, respectively. Pentobarbital, a typical general anesthetic agent with no psychotic symptoms, did not affect the uptake of monoamines, however. Further, neither the glycine transporter 1 nor the glutamate/aspartate transporter was affected by ketamine, indicating that ketamine preferentially inhibits monoamine transporters. Conclusions Ketamine inhibited monoamine transporters expressed in human embryonic kidney cells in a dose-dependent manner. This result suggests that the ketamine-induced inhibition of monoamine transporters might contribute to its psychotomimetic and sympathomimetic effects through potentiating monoaminergic neurotransmission.
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Duerr, Janet S., Jennifer Gaskin, and James B. Rand. "Identified neurons in C. elegans coexpress vesicular transporters for acetylcholine and monoamines." American Journal of Physiology-Cell Physiology 280, no. 6 (2001): C1616—C1622. http://dx.doi.org/10.1152/ajpcell.2001.280.6.c1616.

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We have identified four neurons (VC4, VC5, HSNL, HSNR) in Caenorhabditis elegans adult hermaphrodites that express both the vesicular acetylcholine transporter and the vesicular monoamine transporter. All four of these cells are motor neurons that innervate the egg-laying muscles of the vulva. In addition, they all express choline acetyltransferase, the synthetic enzyme for acetylcholine. The distributions of the vesicular acetylcholine transporter and the vesicular monoamine transporter are not identical within the individual cells. In mutants deficient for either of these transporters, there is no apparent compensatory change in the expression of the remaining transporter. This is the first report of neurons that express two different vesicular neurotransmitter transporters in vivo.
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Gründemann, Dirk, Christian Hahne, Reinhard Berkels, and Edgar Schömig. "Agmatine Is Efficiently Transported by Non-Neuronal Monoamine Transporters Extraneuronal Monoamine Transporter (EMT) and Organic Cation Transporter 2 (OCT2)." Journal of Pharmacology and Experimental Therapeutics 304, no. 2 (2003): 810–17. http://dx.doi.org/10.1124/jpet.102.044404.

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Bhat, Shreyas, Amy Hauck Newman, and Michael Freissmuth. "How to rescue misfolded SERT, DAT and NET: targeting conformational intermediates with atypical inhibitors and partial releasers." Biochemical Society Transactions 47, no. 3 (2019): 861–74. http://dx.doi.org/10.1042/bst20180512.

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Abstract Point mutations in the coding sequence for solute carrier 6 (SLC6) family members result in clinically relevant disorders, which are often accounted for by a loss-of-function phenotype. In many instances, the mutated transporter is not delivered to the cell surface because it is retained in the endoplasmic reticulum (ER). The underlying defect is improper folding of the transporter and is the case for many of the known dopamine transporter mutants. The monoamine transporters, i.e. the transporters for norepinephrine (NET/SLC6A2), dopamine (DAT/SLC6A3) and serotonin (SERT/SLC6A4), have a rich pharmacology; hence, their folding-deficient mutants lend themselves to explore the concept of pharmacological chaperoning. Pharmacochaperones are small molecules, which bind to folding intermediates with exquisite specificity and scaffold them to a folded state, which is exported from the ER and delivered to the cell surface. Pharmacochaperoning of mutant monoamine transporters, however, is not straightforward: ionic conditions within the ER are not conducive to binding of most typical monoamine transporter ligands. A collection of compounds exists, which are classified as atypical ligands because they trap monoamine transporters in unique conformational states. The atypical binding mode of some DAT inhibitors has been linked to their anti-addictive action. Here, we propose that atypical ligands and also compounds recently classified as partial releasers can serve as pharmacochaperones.
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Zhao, Gang, Cheng Bi, Guo-Wei Qin, and Li-He Guo. "Caulis Sinomenii Extracts Activate DA/NE Transporter and Inhibit 5HT Transporter." Experimental Biology and Medicine 234, no. 8 (2009): 976–85. http://dx.doi.org/10.3181/0903-rm-92.

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Caulis Sinomenii (QFT) has analgesic, sedative, and anxiolytic-like actions, and is proven effective for improving drug dependence that is known to be associated with abnormal monoaminergic transmission. We assessed whether QFT would be biologically active in functionally regulating monoamine transporters using CHO cells expressing dopamine transporter (DAT), norepinephrine transporter (NET), or serotonin transporter (SERT) (i.e. D8, N1, or S6 cells, respectively). Here, we showed that its primary extracts, such as QA, QC, QE, QD, and QB (QFT ethanol, chloroform, ethyl acetate, alkaloid-free chloroform, and alkaloid-containing chloroform extract, respectively), and secondary extracts, such as QE-2, − 3, − 5, − 7, QD-1, − 2, − 3, − 4, − 5, and QB-1, − 2, − 3, − 4, − 5 (fractioned from QE, QD, and QB, respectively), in differing degrees, either increased DA/ NE uptake by corresponding D8/N1 cells or decreased 5HT uptake by S6 cells; wherein, QE-2, QD-3, and QE-7 were potent DA/NE uptake activators while both QE-7 and QB-5 were potent 5HT uptake inhibitors. Furthermore, the enhancement of DA/NE uptake was dependent of DAT/NET activity, and the inhibition of 5HT uptake was typical of competition. Thus, QFT extracts, especially QE-2 and QE-7 (both with stronger potencies), are novel monoamine transporter modulators functioning as DAT/ NET activators and/or SERT inhibitors, and would likely improve neuropsychological disorders through regulating monoamine transporters.
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Apparsundaram, Subbu. "Function and Regulation of Monoamine Transporters: Focus on the Norepinephrine Transporter." CNS Spectrums 6, no. 8 (2001): 671–78. http://dx.doi.org/10.1017/s109285290000136x.

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ABSTRACTPresynaptic norepinephrine transporters (NETs) mediate the rapid clearance of norepinephrine from synaptic spaces. NET is a member of the Na+ and Cl− -coupled neurotransmitter transporter gene family, which also includes the serotonin and dopamine transporters. Recent studies reveal that these transporter molecules might be a dynamic component of synaptic plasticity, rather than a constitutive determinant of neurotransmitter levels in synaptic spaces. Recognition that cellular signaling molecules and transporter ligands, including cocaine, amphetamines, and antidepressants, can modify transporter intrinsic activity, trafficking, phosphorylation, and protein levels suggests opportunities for revealing unknown mechanisms of drug action. Control of these properties of transporter function may allow for the development of new strategies to modulate monoaminergic neurotransmission and identify regulatory pathways that may be compromised in psychiatric, neurologic, and neurodegenerative disorders.
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Wagstaff, Ryan, Michael Hedrick, Jun Fan, Paul D. Crowe, and Daniel DiSepio. "High-Throughput Screening for Norepinephrine Transporter Inhibitors Using the FLIPRTetra." Journal of Biomolecular Screening 12, no. 3 (2007): 436–41. http://dx.doi.org/10.1177/1087057106297994.

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Monoamine transporters regulate the concentration of neurotransmitters in the synapse following neurotransmission and are very important drug targets in the pharmaceutical industry. Because of the labor-intensive nature of functional uptake assays using radioactive substrates, high-throughput screening for monoamine transporter inhibitors has been limited to radioligand binding assays. In this article, the authors describe the development of a 384-well, high-throughput functional screening assay for norepinephrine transporter inhibitors using the FLIPRTetra and a recently identified fluorescent substrate, 4-(4-dimethylaminostyryl)- N-methyl-pyridinium (ASP+). ( Journal of Biomolecular Screening 2007:436-441)
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Ramamoorthy, Sammanda, Toni S. Shippenberg, and Lankupalle D. Jayanthi. "Regulation of monoamine transporters: Role of transporter phosphorylation." Pharmacology & Therapeutics 129, no. 2 (2011): 220–38. http://dx.doi.org/10.1016/j.pharmthera.2010.09.009.

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Erdem, Fatma Asli, Marija Ilic, Peter Koppensteiner, et al. "A comparison of the transport kinetics of glycine transporter 1 and glycine transporter 2." Journal of General Physiology 151, no. 8 (2019): 1035–50. http://dx.doi.org/10.1085/jgp.201912318.

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Transporters of the solute carrier 6 (SLC6) family translocate their cognate substrate together with Na+ and Cl−. Detailed kinetic models exist for the transporters of GABA (GAT1/SLC6A1) and the monoamines dopamine (DAT/SLC6A3) and serotonin (SERT/SLC6A4). Here, we posited that the transport cycle of individual SLC6 transporters reflects the physiological requirements they operate under. We tested this hypothesis by analyzing the transport cycle of glycine transporter 1 (GlyT1/SLC6A9) and glycine transporter 2 (GlyT2/SLC6A5). GlyT2 is the only SLC6 family member known to translocate glycine, Na+, and Cl− in a 1:3:1 stoichiometry. We analyzed partial reactions in real time by electrophysiological recordings. Contrary to monoamine transporters, both GlyTs were found to have a high transport capacity driven by rapid return of the empty transporter after release of Cl− on the intracellular side. Rapid cycling of both GlyTs was further supported by highly cooperative binding of cosubstrate ions and substrate such that their forward transport mode was maintained even under conditions of elevated intracellular Na+ or Cl−. The most important differences in the transport cycle of GlyT1 and GlyT2 arose from the kinetics of charge movement and the resulting voltage-dependent rate-limiting reactions: the kinetics of GlyT1 were governed by transition of the substrate-bound transporter from outward- to inward-facing conformations, whereas the kinetics of GlyT2 were governed by Na+ binding (or a related conformational change). Kinetic modeling showed that the kinetics of GlyT1 are ideally suited for supplying the extracellular glycine levels required for NMDA receptor activation.
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Inyushin, M. Y., A. Huertas, Y. V. Kucheryavykh, et al. "L-DOPA Uptake in Astrocytic Endfeet Enwrapping Blood Vessels in Rat Brain." Parkinson's Disease 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/321406.

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Astrocyte endfeet surround brain blood vessels and can play a role in the delivery of therapeutic drugs for Parkinson’s disease. However, there is no previous evidence of the presence of LAT transporter forL-DOPA in brain astrocytes except in culture. Using systemicL-DOPA administration and a combination of patch clamp, histochemistry and confocal microscopy we found thatL-DOPA is accumulated mainly in astrocyte cell bodies, astrocytic endfeet surrounding blood vessels, and pericytes. In brain slices: (1) astrocytes were exposed to ASP+, a fluorescent monoamine analog of MPP+; (2) ASP+taken up by astrocytes was colocalized withL-DOPA fluorescence in (3) glial somata and in the endfeet attached to blood vessels; (4) these astrocytes have an electrogenic transporter current elicited by ASP+, but intriguingly not byL-DOPA, suggesting a different pathway for monoamines andL-DOPA via astrocytic membrane. (5) The pattern of monoamine oxidase (MAO type B) allocation in pericytes and astrocytic endfeet was similar to that ofL-DOPA accumulation. We conclude that astrocytes controlL-DOPA uptake and metabolism and, therefore, may play a key role in regulating brain dopamine level during dopamine-associated diseases. These data also suggest that different transporter mechanisms may exist for monoamines andL-DOPA.
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Dissertations / Theses on the topic "Monoamine transporter"

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Hansson, Stefan R. "The serotonin transporter and vesicular monoamine transporters during development." Lund : Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/68945023.html.

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Holloway, Alexa. "Pharmacodynamics of Monoamine Transporter Releasing Agents and Reuptake Inhibitors." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5880.

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Ligands of the human monoamine transporters encompass a wide range of both illicit and therapeutic drugs that act upon neural circuitry related to reward, motivation, and the processing of salient stimuli. The present study utilizes two methods for analyzing transporter substrates and inhibitors in order to characterize activity and assess potency. The first measures transient changes in intracellular calcium as a surrogate for transporter activity by harnessing the electrical coupling of monoamine transporters and L-type calcium channels. This is used to analyze novel chimera of the strong hDAT inhibitors methylphenidate and 𝛼-PPP in order to assess the contribution of specific moieties to potency. The observed reduction in potency suggests that methylphenidate may bind to the transporter in a manner distinct from 𝛼-PPP, as chimera would otherwise be expected to show similar activity to parent compounds. These results highlight the importance of 𝛼-carbon substituents and the relatively small contribution of beta-carbon groups to inhibitor potency at hDAT, while the lack of activity at hSERT suggests potency is not strongly influenced by beta-carbon or N-alkyl substituents. In order to further characterize drug-transporter interaction, a method was developed to analyze the kinetics of binding and unbinding using both known and novel hNET ligands, including a series of N-alkyl derivatives of 4-methylamphetamine. The study emphasizes the importance of both association and dissociation kinetics to affinity and sets up a methodological framework with two ways for determining Kd, with notable advantages over current models. The results indicate that lengthening the N-alkyl chain of 4-methylamphetamine leads to a decrease in potency and a shift in activity from substrate to blocker, with the results of N-propyl 4-methylamphetamine in particular indicating the potential existence of multiple low-affinity binding sites, each with distinct on and off kinetics. The implications of these results help elucidate the mechanism of action of transporter ligands and set up a framework for future studies that can more specifically classify the interaction between transporters and inhibitors or releasing agents.
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Cameron, Krasnodara. "Conduction states of the human dopamine transporter." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3676.

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Dysregulation of dopaminergic homeostasis has been established as the primary source of numerous neurological disorders including Parkinson’s and drug addiction. A tonic increase of dopamine (DA) in the nucleus accumbens is required for associating everyday events and behaviors with rewards. Yet many addictive exogenous compounds such as amphetamine (AMPH) and cocaine (COC) produce a much greater augmentation of synaptic DA levels that are linked to euphoria and a shift in behavior towards drug seeking. The protein responsible for maintaining extracellular levels of DA is the dopamine transporter (DAT). It is primarily located in the perisynaptic area at terminals of pre-synaptic neurons where its main function is to sequester DA from the extracellular space and to transport it back into the cell, a process that is electrogenic. AMPH and COC directly interact with DAT and alter its ionic currents. Not much is known about the effect of psychostimulant-induced DAT currents on neuronal excitability and neurotransmitter release. We use synthetic chemistry, molecular biology, and biophysics in heterologous expression systems to decipher the actions of drugs of abuse on DAT. Furthermore we demonstrate drug-induced DAT currents can activate Ca2+ channels associated with dopaminergic excitability. Lastly, we focused on investigating drug effects on excitability in a human midbrain dopaminergic cell line. Understanding how psychostimulants interact with DAT to produce the dysfunctional states of the transporter may facilitate the development of unique therapeutic strategies to treat psychostimulant dependence.
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Hojati, Ashkhan. "Pharmacologic profiling of novel compounds via fluorometric analyses of monoamine transporter responses." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5983.

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In humans and other organisms, monoaminergic systems are crucial in neuronal function and behavior. The monoamine transporters (MATs), which can be found on the presynaptic plasma membrane of neurons in the central nervous system (CNS), are crucial in the regulation of neurotransmitter concentration in the synaptic cleft. As the duration and concentration of neurotransmitters in the cleft affect further downstream signaling responses, these proteins are important targets for both understanding neuronal physiology and compounds of interest. Multiple theories exist proponing the contribution of MATs to a variety of mental and neurological disorders, including depression. This theory establishes that depression is caused by imbalances in monoamine neurotransmitters. Compounds such as Fluoxetine (FLX) are classified as selective serotonin reuptake inhibitors (SSRIs), these drugs selectively block the reuptake of neurotransmitters at the serotonin transporter (SERT). Since differences in MAT selectivity of inhibitory compounds are influential to selecting efficacious antidepressant treatments, we utilized a unique fluorescent analysis technique to explore three therapeutic compounds of interest (in-vitro) which contain structural similarity to FLX. Our results confirm the selectivity of FLX at SERT, and classify the novel compounds studied into different potential categories of reuptake inhibitors. We hope these compounds will be studied further to elucidate their potentially therapeutic roles and mitigation of undesired side effects seen in other medications.
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Watson-Siriboe, Abena. "MUTATION OF THE VESICULAR MONOAMINE TRANSPORTER-1 GENE ALTERS ITS PROTEIN PRODUCT." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/77.

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The vesicular monoamine transporter 1 (VMAT1) is essential for storage of monoamines, such as epinephrine and serotonin, in secretory vesicles of neuroendocrine cells. Recently the VMAT1 protein was detected in human and mouse brain, and mutations of the VMAT1 gene at single DNA nucleotides (single nucleotide polymorphisms or SNPs) were associated with schizophrenia. In this study, Chinese hamster ovarian cells were stably transfected with either human VMAT1 DNA (GenBank: #NM_003053.1 or DNA with the Thr4Pro SNP, which results in a threonine to proline change in amino acid number 4 of the VMAT1 protein. Western blot analysis revealed that cells with the SNP produced immunoreactive human VMAT1 proteins of altered molecular size, suggesting that SNP Thr4Pro modifies either folding or processing of the VMAT1 protein. This finding is the first evidence for biochemical consequences of a mutation in the human VMAT1 gene.
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Bhatt, Sandeep. "SEX DIFFERENCES IN DOPAMINE REUPTAKE PATHWAYS OF THE NIGROSTRIATAL DOPAMINERGIC SYSTEM IN MICE." Kent State University / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=kent1164141349.

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Croft, Benjamin. "Examining synaptic vesicle morphology and function in dopamine neurons of mice lacking vesicular monoamine transporter 2." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78342.

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The brain isoform of the vesicular monoamine transporter (VMAT2) packages monoamines into synaptic vesicles (SVs), an essential step in synaptic transmission by central dopamine (DA) neurons. While the modulation of VMAT2 levels influences the amount of DA that can be released, the underlying mechanisms remain unclear. The objective of the present study is to elucidate these mechanisms by examining the SVs of VMAT2 knock out (KO) mice. We used transmission electron microscopy to determine that DA terminals from VMAT2 KO and wild type samples are morphologically indistinguishable from one another. We then monitored the uptake and release of the activity dependent fluorescent dye FM1-43 by VMAT2 KO neurons and found that their SVs cycle, despite being devoid of DA. Our results demonstrate that SV biogenesis and cycling are independent of SV filling, suggesting that one way by which changes in VMAT2 levels could influence is DA release by altering the proportion of SVs that are able to fill.
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Zhou, Mingyan. "Structural and functional analysis of a novel organic cation/monoamine transporter PMAT in the SLC29 family /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/7979.

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Ruiz, Brian A. "Utilizing Voltage-gated Calcium Channels to Assess the Activity of Cathinone Derivatives at Human Monoamine Transporters." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5547.

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Cathinones are psychostimulant compounds heavily implicated as drugs of abuse. They exert their physiological actions at the monoamine transporters, which are responsible for maintaining synaptic neurotransmitter homeostasis. Monoamine transporters produce currents during transport and have been shown to depolarize cell membranes and activate voltage-gated calcium channels in mammalian expression systems. This phenomenon is harnessed in an assay which measures these induced calcium transients, allowing for quantification of pharmacodynamic effects of compounds at monoamine transporters. It is unknown if this electrical coupling occurs in neurons, but the implications if it does are significant. In the current work, fluorescent resonance energy transfer studies of HEK cells expressing hDAT suggest that a subpopulation of monoamine transporters and calcium channels may be interacting directly. Additionally, this work presents calcium assay data comparing several novel methcathinone analogs. Of the compounds tested, a single α-methyl substituent at the α-carbon yields the greatest potency at hDAT. The implications of these results shed light on future psychostimulant studies and further define the physiological relationship of the components of a system used to study these compounds.
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Haapaniemi, T. (Tarja). "Autonomic dysfunction in Parkinson's disease and its correlates to medication and dopamine transporter binding." Doctoral thesis, University of Oulu, 2001. http://urn.fi/urn:isbn:9514259637.

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Abstract Patients with idiopathic Parkinson's disease (PD) may suffer from autonomic nervous system dysfunction even in the early phase of the disease. We assessed the autonomic cardiovascular and sudomotor regulation in de novo PD patients with and without medication. We also measured the dopamine (DAT) and serotonin transporter (SERT) uptake in the PD patients using 2β-carboxymethoxy-3β-(4-iodophenyl)tropane (β-CIT) SPECT and studied the clinical correlates of the uptake. Sixty PD patients were included in the study and randomised to receive levodopa, bromocriptine or selegiline (n=20 in each) as their treatment. Thirty patients were examined with β-CIT SPECT. The results of the patients were compared with those of healthy controls and within the subgroups at different time points. Cardiovascular autonomic regulation was assessed using standard cardiovascular reflex tests at baseline, after six months' medication and following a 6-week washout period. The heart rate (HR) and blood pressure (BP) regulation was impaired in PD patients at baseline, and PD medications modified the responses further. Bromocriptine and selegiline, in contrast to levodopa, increased the orthostatic BP fall and suppressed the BP response to isometric exercise. The long-term cardiovascular autonomic function was evaluated from ambulatory ECG recordings by analysis of traditional spectral and non-spectral components of HR fluctuation together with two-dimensional vector analysis and power-law relationship analysis of the HR dynamics. All spectral measures and the slope of the power-law relationship demonstrated impaired tonic cardiovascular regulation in the PD patients. Sympathetic sudomotor activity was evaluated using the sympathetic skin response (SSR). The major finding was suppression of the SSR amplitudes with an inverse correlation to clinical disability, whereas PD medication seemed to have only minor effects. The changes in amplitude and repetitiveness of the SSRs with normal adaptation suggest deficits at several levels of the SSR reflex arc. DAT uptake, assessed by β-CIT SPECT, was diminished in the striatum and especially the putamen of the PD patients, and correlated with the results of the cardiovascular reflex tests and ambulatory ECG recordings. Simultaneous measurement of SERT binding demonstrated decreased SERT availability in the thalamic and frontal areas. The results demonstrate disturbances of the reflectory and tonic cardiovascular autonomic regulation caused by PD itself. PD medications further modify the reflectory responses. The degenerative process in PD also involves the sympathetic sudomotor pathway. β-CIT SPECT provides a useful method for simultaneous assessment of DAT and SERT binding, demonstrating the deficit of serotonin metabolism in PD.
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Books on the topic "Monoamine transporter"

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Heales, Simon, Simon Pope, Viruna Neergheen, and Manju Kurian. Abnormalities of CSF Neurotransmitters/Folates. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0082.

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The term Neurotansmitter disorder, in the area of metabolic disease, focuses particularly on inborn errors affecting monoamine (dopamine & serotonin), pyridoxal phosphate (B6) and folate metabolism. Whilst there has been considerable focus on these disorders with regards to the paediatric population, it is clear that an increasing number of adult patients are being identified. Adult neurologists need to be aware of the clinical presentation of such patients and the appropriate tests that need to be requested to ensure a correct diagnosis is achieved. CSF profiling, by a specialist laboratory, is often required. This has the ability to very often identify the nature of a primary defect with regards to implementation of appropriate treatment. For some of these disorders, treatment can be effective. This may be in the form of monoamine/vitamin replacement. However there are exceptions, e.g. aromatic amino acid decarboxylase and dopamine transporter deficiencies. There also needs also to be an awareness of the growing list of secondary factors that can cause impaired dopamine and serotonin metabolism.
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Roze, Emmanuel, and Nenad Blau. Biogenic Monoamine Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0031.

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Biogenic monoamine disorders are a group of inherited diseases characterized by a defect in the synthesis, transport, or degradation of catecholamines and serotonin. The phenotype mostly reflects the pattern and severity of the monoamine deficiency. Movement disorders due to cerebral dopamine deficiency are almost always prominent, mostly in the form of dystonia and/or parkinsonism. These disorders are potentially devastating yet treatable. Early diagnosis and treatment are crucial to prevent ongoing brain dysfunction. Detection of hyperphenylalaninemia in a neonate could be a good clue to the diagnosis. Final diagnosis is often based on a detailed biochemical investigation of the cerebrospinal fluid and can be confirmed by molecular analysis. Treatment is aimed at restoring neurotransmitter homeostasis using monoamine precursors, monoamine agonists, and inhibitors of monoamine degradation. It also comprises the control of hyperphenylalaninemia and the prevention of cerebral folate deficiency, when applicable.
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Nielsen, David A., Dmitri Proudnikov, and Mary Jeanne Kreek. The Genetics of Impulsivity. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0080.

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Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.
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Mason, Peggy. Synthesis, Packaging, and Termination of Neurotransmitters. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0012.

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The synthesis, packaging, and termination of action of neurotransmitters are detailed. There are far more varieties of peptide neurotransmitters than there are of low-molecular-weight neurotransmitters. Yet low-molecular-weight neurotransmitters are the ubiquitous workhorses of the nervous system. Acetylcholine, the catecholamines norepinephrine and dopamine, serotonin, glutamate, and GABA are examined in some depth. The vesicular transporters that carry low-molecular-weight neurotransmitters from the cytoplasm into synaptic vesicles are covered. The role of monoamines in affect and mood and the psychotropic effects of monoaminergic drugs are discussed. Principles of catecholamine synthesis are applied to understand phenylketonuria. Uptake of monoamines into neurons is discussed in the context of amphetamine, cocaine, and other drugs of abuse. Stiff-person syndrome, which results from an impairment of GABA synthesis, is introduced. The modes of action for peptide and gaseous neurotransmitters are briefly covered.
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Pearl, Phillip L., and William P. Welch. Pediatric Neurotransmitter Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0059.

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The pediatric neurotransmitter disorders represent an enlarging group of neurological syndromes characterized by inherited abnormalities of neurotransmitter synthesis, metabolism, and transport. Disorders involving monoamine synthesis include guanosine triphosphate cyclohydrolase deficiency (Segawa disease or classical Dopa-responsive dystonia as the heterozygous form), aromatic amino acid decarboxylase deficiency, tyrosine hydrolase deficiency, sepiapterin reductase deficiency, and disorders of tetrahydrobiopterin synthesis. These disorders can be classified according to whether they feature elevated serum levels of phenylalanine. Disorders of γ-amino butyric acid (GABA) metabolism include succinic semialdehyde dehydrogenase deficiency and GABA-transaminase deficiency. Glycine encephalopathy is typically manifested by refractory neonatal seizures due to a defect in the glycine degradative pathway. Pyridoxine-responsive seizures have now been associated with deficiency of α-aminoadipic semialdehyde dehydrogenase as well as a variants requiring therapy with pyridoxal-5-phosphate and folinic acid.
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Miao-Kun, Sun, ed. Cognitive sciences research progress. Nova Science Publishers, 2009.

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Book chapters on the topic "Monoamine transporter"

1

Sealover, Natalie R., and Eric L. Barker. "Monoamine Transporter Pathologies." In Neurochemical Mechanisms in Disease. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7104-3_6.

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Marchiori, Deborah, and Silvia Uccella. "Vesicular Monoamine Transporter 2 (VMAT2)." In Encyclopedia of Pathology. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-28845-1_5320-1.

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Simmler, Linda D. "Monoamine Transporter and Receptor Interaction Profiles of Synthetic Cathinones." In Current Topics in Neurotoxicity. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78707-7_6.

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Meyer, Jeffrey H. "Monoamine Oxidase A and Serotonin Transporter Imaging with Positron Emission Tomography." In PET and SPECT of Neurobiological Systems. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-42014-6_25.

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Meyer, Jeffrey H. "Monoamine Oxidase A and Serotonin Transporter Imaging with Positron Emission Tomography." In PET and SPECT of Neurobiological Systems. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-53176-8_26.

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German, Dwight C., and Patricia K. Sonsalla. "A Role for the Vesicular Monoamine Transporter (VMAT2) in Parkinson’s Disease." In Advances in Behavioral Biology. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0179-4_13.

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Sucic, Sonja, and Heinz Bönisch. "Classical Radioligand Uptake and Binding Methods in Transporter Research: An Emphasis on the Monoamine Neurotransmitter Transporters." In Neuromethods. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3765-3_1.

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Lohoff, Falk W. "Genetic Variants in the Vesicular Monoamine Transporter 1 (VMAT1/SLC18A1) and Neuropsychiatric Disorders." In Methods in Molecular Biology. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-700-6_9.

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Sitte, H. H., and M. Freissmuth. "Monoamine Transporters in the Brain." In Handbook of Neurochemistry and Molecular Neurobiology. Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-30380-2_17.

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Trendelenburg, U., L. Cassis, M. Grohmann, and A. Langeloh. "The functional coupling of neuronal and extraneuronal transport with intracellular monoamine oxidase." In Monoamine Oxidase Enzymes. Springer Vienna, 1987. http://dx.doi.org/10.1007/978-3-7091-8901-6_6.

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