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1 (5-HT1) on pericytes, despite the absence of monoamines.
2 pendent modulation of cortical efficiency by monoamines.
3 ades monoamine neurotransmitters and dietary monoamines.
4 tress, influences apoptosis, and metabolizes monoamines.
5 ing and eliminated the inhibitory actions of monoamines.
6       However, little is known regarding how monoamines affect OFC neuron excitability or whether thi
7 el tone adapts to the loss of neuron-derived monoamines after spinal cord injury (SCI) in rats.
8 e area, glial activation, CNS cytokines, and monoamine and amino acid neurotransmitters were quantifi
9                However, individuals who take monoamine and diamine oxidase inhibitors drugs should be
10                                          The monoamine and neuropeptide networks exhibit distinct top
11 lates nociception through the interaction of monoamine and neuropeptide signaling pathways.
12  diamines that are selectively detected over monoamines and alpha-amino acids.
13 xicity results in long-lasting depletions of monoamines and changes in basal ganglia function.
14                            AANAT1 acetylates monoamines and inactivates them, and we found that AANAT
15 synaptic volume transmission, especially via monoamines and neuropeptides, is also critical to brain
16                    Here we show that natural monoamines and synthetic amines inhibit pDC activation b
17                              The presence of monoamines and their cofactors (the pterins and vitamin
18 (HPLC) approaches to determine CSF levels of monoamines and their cofactors.
19 S9-2) plays a key modulatory role in opioid, monoamine, and other G-protein-coupled receptor response
20         The OFC is extensively innervated by monoamines, and drugs that target monoamine receptors ha
21 er neuromodulatory control by acetylcholine, monoamines, and other signaling molecules.
22 these studies could potentially affect other monoamines, and the scarcity of imaging evidence on dopa
23                                              Monoamines are analyzed by HPLC with coulometric electro
24           Together, these findings show that monoamines are important modulators of lOFC excitability
25                    We found that invasion of monoamine, basal forebrain, thalamocortical, and cortico
26 ssant, imipramine, and a rapidly acting, non-monoamine-based antidepressant, ketamine, in mice subjec
27 fully modulating the amphiphilic nature of a monoamine-based GAEL, we can generate a potent triamino
28    We compared the effects of a conventional monoamine-based tricyclic antidepressant, imipramine, an
29 r AANAT1 and astrocytes in the regulation of monoamine bioavailability and homeostatic sleep.
30 predictive of reduced central nervous system monoamines by bioinformatics analyses and confirmed by h
31                  We have mapped the putative monoamine connections, as well as a subset of neuropepti
32  (Tph2, SERT, and Pet-1) genes, and midbrain monoamine content in mice raised under control Equinox (
33 act and the mode of action involves abnormal monoamine content in trout.
34                                              Monoamines, cytokines, glutamate, GABA and other central
35                                    All three monoamines decreased current-evoked spike firing of lOFC
36 nd solitary locusts co-injected by these two monoamines displayed the same tendency as the olfactory
37 man patient-derived xenograft lines, how the monoamine dopamine influences GBM cells.
38                              The role of the monoamines dopamine (DA) and serotonin (5HT) and the mon
39 ely, it is thought that, with one exception, monoamines (dopamine, serotonin, and norepinephrine) sig
40                                    Resultant monoamine dysregulation may underlie SAD symptomatology
41 ses of d-amphetamine (AMPH), which increases monoamine efflux in the mPFC.
42 erived hypothesis that moderate increases in monoamine efflux would enhance attractor stability, wher
43 are less efficacious than others in inducing monoamine efflux).
44  2 (VMAT2) substrate that selectively traces monoamine exocytosis in both neuronal cell culture and b
45  helicates of different sizes from a primary monoamine, Fe(II) ions, and dialdehyde ligand strands th
46 enetic link for cannabis regulation of brain monoamine function.
47      The electrochemical similarity of these monoamines, however, confounds real-time measurements of
48 tered on neurochemical deficits, such as the monoamine hypothesis, research toward this goal has shif
49             Histamine (HA), a wake-promoting monoamine implicated in stress-related arousal states, i
50 ich is required for the vesicular storage of monoamines in both SVs and LDCVs.
51 ion among their symptoms, the implication of monoamines in depression, and the hypothesis that PrP(C)
52                         Based on the role of monoamines in reconfiguring invertebrate networks, and d
53 actions by elevating extracellular levels of monoamines in the brain.
54  most efficient deamination takes place when monoamine is in the zwitterionic form (pH 9-11) or diami
55 -amines were tried for polymer modification: monoamine Jeffamine M 1000 used previously in some resea
56 pocalins with tick lipocalins that sequester monoamines, leukotrienes and fatty acids.
57 nding on the modulatory action of harmane on monoamine levels and could potentially be of therapeutic
58 e hypothesis that venlafaxine perturbs brain monoamine levels and disrupts molecular responses essent
59 ol behavioral flexibility, we found elevated monoamine levels in the PFC of CD38(-/-) adult mice.
60 arbolines including harmane modulate central monoamine levels partly through monoamine oxidase (MAO)
61 ver, TPH2 expression and activity as well as monoamine levels were unchanged in the projection areas
62 ce attractor stability, whereas high frontal monoamine levels would severely diminish it.
63 mpared intra-PFC opioid manipulations with a monoamine manipulation (d-amphetamine), in two sucrose-r
64          Computational theories propose that monoamines may exert bidirectional (concentration-depend
65              These results indicate both low monoamine metabolism and neuronal membrane dysfunction a
66 ed a genome-wide association study (GWAS) of monoamine metabolite (MM) levels in cerebrospinal fluid
67 ramine (4-hydroxyphenethylamine), which is a monoamine metabolized by monoamine oxidase (MAO), exists
68 es dopamine (DA) and serotonin (5HT) and the monoamine-metabolizing enzyme monoamine oxidase A (MAOA)
69 macologic profile that combines dose-related monoamine modulation with phosphorylation of intracellul
70 work analysis for GABA, butyrate, glutamate, monoamines, monosaturated fatty acids, and inflammasome
71 it distinct topological properties, with the monoamine network displaying a highly disassortative sta
72 ion in embryonic mid-hindbrain regions where monoamine neurons emerge.
73 nd encodes a receptor (TAAR1) that modulates monoamine neurotransmission and at which MA serves as an
74 holinergic enzymes and receptors, markers of monoamine neurotransmission as well as steroid-related t
75 on mechanism for the biological reduction in monoamine neurotransmission in Parkinson's patients.
76 drobiopterin (THB), an essential cofactor in monoamine neurotransmitter biosynthesis.
77 t currently available antidepressants target monoamine neurotransmitter function.
78        Norepinephrine (NE) is a key biogenic monoamine neurotransmitter involved in a wide range of p
79                           Dopamine (DA) is a monoamine neurotransmitter responsible for regulating a
80                           Dopamine (DA) is a monoamine neurotransmitter responsible for the maintenan
81  regulates neurotransmission by the biogenic monoamine neurotransmitter serotonin (5-HT, 5-hydroxytry
82                                          The monoamine neurotransmitter serotonin (5-hydroxytryptamin
83 termination of ultra-trace concentrations of monoamine neurotransmitter such as noradrenaline (NA) in
84 lase (AADC) deficiency is an inborn error of monoamine neurotransmitter synthesis, which results in d
85 tetrahydrobiopterin, a critical cofactor for monoamine neurotransmitter synthesis.
86 (MAOA), a mitochondrial enzyme that degrades monoamine neurotransmitters and dietary amines, in strom
87 (MAOA), a mitochondrial enzyme that degrades monoamine neurotransmitters and dietary amines.
88 MAOA), a mitochondria-bound enzyme, degrades monoamine neurotransmitters and dietary monoamines.
89 ng DMT at concentrations comparable to known monoamine neurotransmitters and raise the possibility th
90                                              Monoamine neurotransmitters are among the hundreds of si
91                                              Monoamine neurotransmitters are stored in both synaptic
92 ical, in-vitro application for extracellular monoamine neurotransmitters detection in living cells.
93  and amphetamines, act primarily through the monoamine neurotransmitters dopamine (DA), norepinephrin
94 atients fail to produce normal levels of the monoamine neurotransmitters dopamine and serotonin, and
95 al gland, were similar to those of canonical monoamine neurotransmitters including serotonin.
96             Modulation of neural activity by monoamine neurotransmitters is thought to play an essent
97                                              Monoamine neurotransmitters such as serotonin, dopamine,
98 othesis that genomic regions associated with monoamine neurotransmitters would be highly differentiat
99 in-binding site of SULT1A3, which sulfonates monoamine neurotransmitters, is modeled on that of 1A1 a
100 cus coeruleus (LC) and dorsal raphe (DR) are monoamine nuclei implicated in stress-related disorders.
101 f aversive stimuli and inhibitory control of monoamine nuclei.
102 uilding block, iron(II) chloride, and either monoamines or a diamine.
103 f aromatic l-amino acids to produce aromatic monoamines or aromatic acetaldehydes, respectively.
104 s nearly doubled and inhibition of firing by monoamines or ML297 was lost.
105 ly demonstrated direct evidence of increased monoamine oxidase (MAO) activity in the brain of a simia
106 tonin 5-HT1A receptor antagonist) as well as monoamine oxidase (MAO) and functional binding assays we
107               Previous studies have utilized monoamine oxidase (MAO) and L-3,4-dihydroxyphenylalanine
108 uate its potential to visualize and quantify monoamine oxidase (MAO) B activity in vivo.
109 late central monoamine levels partly through monoamine oxidase (MAO) inhibition.
110  endogenous imidazoline ligand agmatine, the monoamine oxidase (MAO) inhibitor harmane, the alpha(2)-
111 at cigarette smoke constituents that inhibit monoamine oxidase (MAO) may increase the reinforcing val
112                                              Monoamine oxidase (MAO) metabolizes cytosolic dopamine (
113                              The flavoenzyme monoamine oxidase (MAO) regulates mammalian behavioral p
114 lamine), which is a monoamine metabolized by monoamine oxidase (MAO), exists widely in plants, animal
115            Tryptophan hydroxylase (TPH1) and monoamine oxidase (MAO-A) are the key enzymes for the sy
116       Drug interaction between inhibitors of monoamine oxidase (MAOIs) and selective serotonin (5-hyd
117           However, it has been reported that monoamine oxidase A (MAO A, a major neurotransmitter-deg
118                                              Monoamine oxidase A (MAO-A) is an important brain enzyme
119                                              Monoamine oxidase A (MAO-A) is an important enzyme on th
120 o counter the effects of the 40% increase in monoamine oxidase A (MAO-A) levels that occurs during PP
121  One such biological abnormality is elevated monoamine oxidase A (MAO-A) levels, which occurs in the
122                                              Monoamine oxidase A (MAOA) activity was associated with
123 g RNA (lncRNA), acting as a regulator of the monoamine oxidase A (MAOA) gene in the brain, and named
124  (5HT) and the monoamine-metabolizing enzyme monoamine oxidase A (MAOA) have been repeatedly implicat
125 y, we identify for the first time a role for monoamine oxidase A (MAOA) in NPC.
126                               We report that monoamine oxidase A (MAOA) is a clinically and functiona
127                                              Monoamine oxidase A (MAOA) is a mitochondrial enzyme tha
128                The rs1137070 polymorphism of monoamine oxidase A (MAOA) is associated with alcoholism
129 ohorts of Finnish prisoners, revealed that a monoamine oxidase A (MAOA) low-activity genotype (contri
130 g growth differentiation factor-3 (GDF3) and monoamine oxidase A (MAOA) that is known to degrade nora
131  6 member 2 (SLC6A2), an NE transporter, and monoamine oxidase A (MAOA), a degradation enzyme.
132                                              Monoamine oxidase A (MAOA), a mitochondria-bound enzyme,
133 cancer (PCa) exhibit increased expression of monoamine oxidase A (MAOA), a mitochondrial enzyme that
134           Here, we show that upregulation of monoamine oxidase A (MAOA), a mitochondrial enzyme that
135 rine secretion; P < 0.01), with no effect on monoamine oxidase A (serotonin catabolism), serotonin re
136  NIRKO mice also exhibit increased levels of monoamine oxidase A and B (MAO A and B) leading to incre
137                 In a screening for potential monoamine oxidase A and B inhibition ciproxifan showed e
138 ted high selectivity (>160x) against related monoamine oxidase A and B.
139  form (sVAP-1) accounts for most circulating monoamine oxidase activity, has insulin-like effects, an
140 o competitive MPP(+)-dependent inhibition of monoamine oxidase activity.
141  (AD), i.e., acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), a series of multitarget lig
142        A set of drugs was further studied in monoamine oxidase B (MAO-B) and cyclooxygenase-1 (COX-1)
143 l) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10
144              Illudinine was found to inhibit monoamine oxidase B (MAO-B) with an IC(50) of 18 +/- 7.1
145 e, competitive, and reversible inhibitors of monoamine oxidase B (MAO-B).
146 was found to suppress the gene expression of monoamine oxidase B (MAOB) in the brain of wild-type but
147 tural comparisons with human metabolites and monoamine oxidase B (MAOB) was identified as the putativ
148 example of a biorelevant synthetic model for monoamine oxidase B activity.
149 onoamine oxidases with slight preference for monoamine oxidase B in both species.
150 hydrogen peroxide (H(2)O(2)) originated from monoamine oxidase B in severe reactive astrocytes causes
151   We report the effects of the addition of a monoamine oxidase B inhibitor, rasagiline, to antidepres
152 est placebo-controlled clinical trial of the monoamine oxidase B inhibitor, rasagiline, we examined h
153 his, a number of highly potent and selective monoamine oxidase B inhibitors were identified.
154 dowed with potent, selective, and reversible monoamine oxidase B inhibitory activity is a clinically
155                                 Accordingly, monoamine oxidase blockers pargyline and l-deprenyl had
156 mine (2, MBA236) as a new cholinesterase and monoamine oxidase dual inhibitor.
157                              MAOB, a crucial monoamine oxidase for dopamine metabolism, triggers oxid
158                         Myelosuppression and monoamine oxidase inhibition (MAOI) are key independent
159 iggers lethal phenethylamine poisoning after monoamine oxidase inhibitor administration.
160                          While tricyclic and monoamine oxidase inhibitor medications were associated
161                                              Monoamine oxidase inhibitors (MAOIs) exert therapeutic a
162 ects on outcomes compared with waitlist were monoamine oxidase inhibitors (SMD -1.01, 95% credible in
163 ts [TCA], atypical antidepressants [AA], and monoamine oxidase inhibitors [MAOI]), age, sex, smoking,
164 idepressants (eg, tricyclic antidepressants, monoamine oxidase inhibitors) were excluded.
165 reated with beta-blockers, ACE inhibitors or monoamine oxidase inhibitors, in children under 5 years
166  and several related synthetic analogues are monoamine oxidase inhibitors, which is the first reporte
167 es was synthesized and screened toward human monoamine oxidase isoforms (hMAO-A and hMAO-B).
168                         The flavin-dependent monoamine oxidase LSD1 (lysine-specific demethylase 1, a
169 g sites for [(18)F]AV-1451, such as neuronal monoamine oxidase or neuromelanin.
170 re, we demonstrate that AMX-2 is the primary monoamine oxidase that metabolizes 5-HT in C. elegans, a
171  to 3,4-dihydroxymandelic acid (DHMA) by the monoamine oxidase TynA and the aromatic aldehyde dehydro
172 ptom, aged <60 years) other medications (eg, monoamine oxidase type B inhibitors [MAOBIs], amantadine
173 gether with organic cation transporter 3 and monoamine oxidase type B, two key proteins for DA uptake
174 cascade consisting of the ATHase, the GDH, a monoamine oxidase, and a catalase leads to the productio
175 d by the transaminase is not affected by the monoamine oxidase, and highlights the potential of this
176 ine oxidase, copper containing 3), a surface monoamine oxidase, as a new marker of myofibroblasts by
177 r has been reported to bind to neuromelanin, monoamine oxidase, calcifications, iron, leptomeningeal
178 ethyl transferase (COMT) and two isoforms of monoamine oxidase--modulated degree of belief learning a
179 ompanied by an increase in the expression of monoamine oxidase-A (MAO-A) and MAO-B in the lateral OFC
180                                              Monoamine oxidase-A (MAO-A) is a treatment target in neu
181       Here we report that high expression of monoamine oxidase-A (MAO-A) is associated with positive
182  study examined how the mitochondrial enzyme monoamine oxidase-A (MAO-A), which produces hydrogen per
183 eas was similarly modulated by inhibition of monoamine oxidase-A and was reduced in animals with indu
184 R antagonist or after incubation with MAO-A (monoamine oxidase-A).
185 -serotonin and increased after inhibition of monoamine oxidase-A, the main enzyme responsible for ser
186                                              Monoamine oxidase-B inhibitors and dopamine agonists can
187                                    Measuring monoamine oxidase-B with neuroimaging and glial fibrilla
188 arins were designed, prepared, and tested as monoamine oxidases (MAOs) and acetyl- and butyryl-cholin
189                The resurgence of interest in monoamine oxidases (MAOs) has been fueled by recent corr
190  carbonyl reductases (CREDs), hydrolases and monoamine oxidases (MAOs), providing a comprehensive ove
191 ty towards acetyl/butyrylcholinesterases and monoamine oxidases A/B as well as the histamine H3 recep
192 enine dinucleotide (FAD) dependent family of monoamine oxidases and is vital in regulation of mammali
193                               As the H3R and monoamine oxidases are all capable of affecting neurotra
194 M1 family is homologous to the mitochondrial monoamine oxidases MAO-A/B and produces hydrogen peroxid
195 omolar concentration range for human and rat monoamine oxidases with slight preference for monoamine
196 and tested for inhibitory activities against monoamine oxidases.
197 terases, N-methyl-D-aspartate receptors, and monoamine oxidases.
198  PPB, a dietary supplement kit consisting of monoamine precursor amino acids and dietary antioxidants
199   2-AG also inhibits locomotion in remodeled monoamine receptor mutant animals designed to measure th
200                                         This monoamine-receptor activity causes pericytes to locally
201 oxia owing to paradoxical excess activity of monoamine receptors (5-HT1) on pericytes, despite the ab
202 ervated by monoamines, and drugs that target monoamine receptors have been used to treat a number of
203                                Inhibition of monoamine receptors or of AADC, or even an increase in i
204  that the loss of the kinase may dysregulate monoamine receptors within these neurons, whose activity
205                                Non-classical monoamine recognition evolved in two steps: an ancestral
206 aggression, but a mechanistic account of how monoamines regulate antisocial motives remains elusive.
207                 This mechanism may extend to monoamine release in central neurons or in the enteric n
208 may mediate pro-social effects by modulating monoamine release in limbic and cortical areas, which wa
209 DA, confirming the direct effects of 2-AG on monoamine release.
210 ylenedioxymethamphetamine (MDMA) is a potent monoamine releaser that produces an acute euphoria in mo
211                               MDMA, a potent monoamine-releaser with particularly pronounced serotoni
212        Receptor activation in the absence of monoamines results from the production of trace amines (
213 dosing with dasotraline, a long-acting, dual monoamine reuptake inhibitor, may be a safe and efficaci
214 s a novel neurogenic compound independent of monoamine reuptake pathways.
215                                              Monoamine serotonin (5HT) has been linked to aggression
216            The membrane transporters for the monoamines serotonin (SERT) and dopamine (DAT) are promi
217                                          The monoamines serotonin and dopamine are key regulators of
218 nduced by brainstem neurons that release the monoamines serotonin and noradrenaline, and local vessel
219 s such as glutamate, neuromodulators such as monoamines signal changes in firing rate.
220  developmental periods that are sensitive to monoamine signaling and impact adult behaviors of releva
221   Here we test the hypothesis that increased monoamine signaling during development causes these para
222 nction as a consequence of increased P22-P41 monoamine signaling might underlie altered aggression.
223 icinus lipocalins have the potential to bind monoamines similar to other tick species previously repo
224                          The clinically safe monoamine stabilizer (-)-OSU6162 (OSU6162) restores dopa
225 s in specific defects in peptide hormone and monoamine storage and regulated secretion.
226 heir cognate substrates and sustain cellular monoamine stores even during neuronal activity.
227 al fluid-contacting (CSF-c) cells containing monoamines such as dopamine (DA) and serotonin (5-HT) oc
228 tion of hindbrain patterning genes can alter monoamine system development and thereby produce forebra
229                                          The monoamine system in the prefrontal cortex has been impli
230 neuropsychiatric disorders, we characterized monoamine systems in relation to forebrain neurogenesis
231 lsivity and motivation relative to PFC-based monoamine systems.
232 ress, facilitates apoptosis, and metabolizes monoamines, therapeutics opposing these processes are pr
233 siology of depression, a paradigm shift from monoamine to glutamatergic neurotransmission, thus makin
234 amily of transporters, mediates transport of monoamines to synaptic vesicles and storage organelles i
235                                      Current monoamine transmission modulating therapeutics, even wit
236  the effort-related effects of the vesicular monoamine transport (VMAT-2) inhibitor tetrabenazine (TB
237 iduals with BPD and leads to marked increase monoamine transport in vitro.
238 ro, with the Ile allele leading to increased monoamine transport into presynaptic vesicles.
239 hus, current knowledge about the kinetics of monoamine transport is sufficiently detailed to provide
240 afficking domain of the Drosophila vesicular monoamine transporter (DVMAT), which is required for the
241                                              Monoamine transporter (MAT) ligands that allosterically
242  cation 3 transporter (OCT3)/plasma membrane monoamine transporter (PMAT) inhibitor, increased the 5-
243 ed bacterial homologues of the rat vesicular monoamine transporter (rVMAT2).
244  pharmacological inhibition of the vesicular monoamine transporter (VMAT) blocks amphetamine-induced
245                                    Vesicular monoamine transporter (VMAT), a member of the largest su
246 hloroamphetamine (pCA), acting via vesicular monoamine transporter (VMAT), and a charged VMAT, substr
247 repinephrine transporter (NET) and vesicular monoamine transporter (VMAT-1) was evaluated immunohisto
248 s demonstrate that the presynaptic vesicular monoamine transporter 1 (VMAT1) Thr136Ile (rs1390938) po
249           TH1-S31E associated with vesicular monoamine transporter 2 (VMAT2) and alpha-synuclein in n
250    We previously reported that the vesicular monoamine transporter 2 (VMAT2) is physically and functi
251 neurons projecting to the LHb lack vesicular monoamine transporter 2 (VMAT2) mRNA, and there is littl
252 lacetic acid (DOPAC)/DA ratio, and vesicular monoamine transporter 2 (VMAT2) protein.
253 e neurotransmitter 200 (FFN200), a vesicular monoamine transporter 2 (VMAT2) substrate that selective
254 coordinated activity of astroglial vesicular monoamine transporter 2 (VMAT2) together with organic ca
255  for the serotonin transporter and vesicular monoamine transporter 2 (VMAT2).
256 AC)-mediated overexpression of the vesicular monoamine transporter 2 (VMAT2; Slc18a2).
257  than the dopamine transporter and vesicular monoamine transporter 2 defects, suggesting upregulation
258 8854) is a novel, highly selective vesicular monoamine transporter 2 inhibitor that demonstrated favo
259 omography (PET) radioligand to the vesicular monoamine transporter 2, (VMAT2), [(11)C]dihydrotetraben
260 ncludes tyrosine hydroxylase (TH), vesicular monoamine transporter 2, and the norepinephrine transpor
261 d genes tyrosine hydroxylase (TH), vesicular monoamine transporter 2, dopamine transporter and aldehy
262 cular acetylcholine transporter or vesicular monoamine transporter 2.
263             Although an influence of CAPS on monoamine transporter function and on vesicle acidificat
264  an antidepressive agent and a non-selective monoamine transporter inhibitor that blocks the reuptake
265                              Dichloropane, a monoamine transporter ligand, enables targeting of dense
266 ethylenedioxyamphetamine analogs bind at the monoamine transporter orthosteric binding site by adopti
267 on reveals the subcellular distribution of a monoamine transporter protein in the axons of a single,
268  requires metabolism to the amphetamine-like monoamine transporter substrate phenmetrazine (PM) to pr
269                                    Vesicular monoamine transporter type 2 (VMAT2) imaging with PET al
270  ([(11)C]DTBZ) binding to striatal vesicular monoamine transporter type 2 (VMAT2) in cocaine abusers
271                                The vesicular monoamine transporter type 2 (VMAT2), an important regul
272 BZ), a novel radiotracer targeting vesicular monoamine transporter type 2 (VMAT2), has been proven as
273 toradiographic measures of DAT and vesicular monoamine transporter type 2 (VMAT2), striatal dopamine,
274             The mean reductions of vesicular monoamine transporter type 2 density for the caudate, pu
275 hydrotetrabenazine (DTBZ; reflects vesicular monoamine transporter type 2), ex vivo quantification of
276 ministration of the VMAT-2 (type-2 vesicular monoamine transporter) inhibitor tetrabenazine (9,10-dim
277  doses of deutetrabenazine-a novel vesicular monoamine transporter-2 inhibitor-in patients with tardi
278 rboxylase, the DA transporter, and vesicular monoamine transporter-2 with EGFP in midbrain dopaminerg
279 ster ovary cells expressing either vesicular monoamine transporter.
280 in receptors (e.g., serotonin receptors) and monoamine transporters (i.e., serotonin, dopamine, and n
281                                              Monoamine transporters (MATs) regulate neurotransmission
282 pports the concept that uptake and efflux at monoamine transporters are asymmetric processes that can
283 C, and HHMC were substrate-type releasers at monoamine transporters as determined in vitro, but only
284                             The plasmalemmal monoamine transporters clear the extracellular space fro
285 loiting structural templates known to target monoamine transporters for dopamine, norepinephrine, and
286 esults provide new insights into the role of monoamine transporters in autophagy regulation and ident
287 nal activities of the compounds at all three monoamine transporters in native brain tissue and cells
288 that define substrates and inhibitors at the monoamine transporters is critical to elucidating the me
289   The serotonin transporter (SERT) and other monoamine transporters operate in either a forward trans
290 ate fast-acting currents, I suggest that the monoamine transporters should be considered as ionotropi
291 ed pore" mechanism in the mammalian synaptic monoamine transporters, and the archaeal GltPh, which is
292 r (LeuT) is a bacterial homolog of the human monoamine transporters, which are important pharmaceutic
293 king mechanism is unique to DAT or common to monoamine transporters.
294 eads to increased activity of both vesicular monoamine transporters.
295 y-five studies (29 DAT, 6 AADC, no vesicular monoamine type 2 studies) with 356 MSA-P patients, 204 P
296 drotetrabenazine ((11)C-DTBZ) is a vesicular monoamine type 2 transporter PET ligand that allows asse
297 mino acid decarboxylase (AADC), or vesicular monoamine type 2 were investigated.
298  with two clinically relevant compounds: the monoamine uptake inhibitor bupropion and the dopamine an
299 e ability of acute administration of various monoamine uptake inhibitors to reverse the effects of TB
300 tive action of acetylcholine (ACh), GABA and monoamines, which lead to transitions between primary br

 
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