ライフサイエンスコーパス: monoamine

1 pendent modulation of cortical efficiency by monoamines.

2 ades monoamine neurotransmitters and dietary monoamines.

3 tress, influences apoptosis, and metabolizes monoamines.

4 ovides unique tools to assess the release of monoamines.

5 ing and eliminated the inhibitory actions of monoamines.

6 /reserpine on sleep are mediated by multiple monoamines.

7 (5-HT1) on pericytes, despite the absence of monoamines.

8 However, little is known regarding how monoamines affect OFC neuron excitability or whether thi

9 el tone adapts to the loss of neuron-derived monoamines after spinal cord injury (SCI) in rats.

10 In all, we demonstrate that monoamine agonists can prevent disease in a vertebrate m

11 e area, glial activation, CNS cytokines, and monoamine and amino acid neurotransmitters were quantifi

12 However, individuals who take monoamine and diamine oxidase inhibitors drugs should be

13 itors, which show specificity for VAP-1 over monoamine and diamine oxidases.

14 The monoamine and neuropeptide networks exhibit distinct top

15 lates nociception through the interaction of monoamine and neuropeptide signaling pathways.

16 ode is sensitive and robust enough to detect monoamine and purine molecules from frontal cortex and s

17 trode, tissue content was analyzed for seven monoamine and two purine molecules, which were resolved

18 diamines that are selectively detected over monoamines and alpha-amino acids.

19 xicity results in long-lasting depletions of monoamines and changes in basal ganglia function.

20 Monoamines and neuropeptides interact to modulate most b

21 synaptic volume transmission, especially via monoamines and neuropeptides, is also critical to brain

22 Here we show that natural monoamines and synthetic amines inhibit pDC activation b

23 showed no overt abnormalities, the uptake of monoamines and the neurotoxin 1-methyl-4-phenylpyridiniu

24 The presence of monoamines and their cofactors (the pterins and vitamin

25 (HPLC) approaches to determine CSF levels of monoamines and their cofactors.

26 S9-2) plays a key modulatory role in opioid, monoamine, and other G-protein-coupled receptor response

27 Reserpine depletes monoamines, and causes depression and hypoactivity in hu

28 The OFC is extensively innervated by monoamines, and drugs that target monoamine receptors ha

29 these studies could potentially affect other monoamines, and the scarcity of imaging evidence on dopa

30 Monoamines are analyzed by HPLC with coulometric electro

31 Together, these findings show that monoamines are important modulators of lOFC excitability

32 We found that invasion of monoamine, basal forebrain, thalamocortical, and cortico

33 ssant, imipramine, and a rapidly acting, non-monoamine-based antidepressant, ketamine, in mice subjec

34 fully modulating the amphiphilic nature of a monoamine-based GAEL, we can generate a potent triamino

35 We compared the effects of a conventional monoamine-based tricyclic antidepressant, imipramine, an

36 predictive of reduced central nervous system monoamines by bioinformatics analyses and confirmed by h

37 tivation of kappa-opioid receptors (KORs) in monoamine circuits results in dysphoria-like behaviors a

38 We have mapped the putative monoamine connections, as well as a subset of neuropepti

39 act and the mode of action involves abnormal monoamine content in trout.

40 Monoamines, cytokines, glutamate, GABA and other central

41 All three monoamines decreased current-evoked spike firing of lOFC

42 nd solitary locusts co-injected by these two monoamines displayed the same tendency as the olfactory

43 The role of the monoamines dopamine (DA) and serotonin (5HT) and the mon

44 ely, it is thought that, with one exception, monoamines (dopamine, serotonin, and norepinephrine) sig

45 odel complex brain disorders associated with monoamine dysregulation.

46 ses of d-amphetamine (AMPH), which increases monoamine efflux in the mPFC.

47 erived hypothesis that moderate increases in monoamine efflux would enhance attractor stability, wher

48 2 (VMAT2) substrate that selectively traces monoamine exocytosis in both neuronal cell culture and b

49 helicates of different sizes from a primary monoamine, Fe(II) ions, and dialdehyde ligand strands th

50 e to drugs bi-directionally modulating brain monoamines, generally paralleling rodent and clinical fi

51 The electrochemical similarity of these monoamines, however, confounds real-time measurements of

52 ich is required for the vesicular storage of monoamines in both SVs and LDCVs.

53 ion among their symptoms, the implication of monoamines in depression, and the hypothesis that PrP(C)

54 Monoamines, including dopamine (DA), have been linked to

55 monoamine transporter (VMAT) that repackages monoamines into presynaptic vesicles, resulted in an inc

56 transporter 2 (VMAT2) catalyzes transport of monoamines into storage vesicles in a process that invol

57 most efficient deamination takes place when monoamine is in the zwitterionic form (pH 9-11) or diami

58 -amines were tried for polymer modification: monoamine Jeffamine M 1000 used previously in some resea

59 pocalins with tick lipocalins that sequester monoamines, leukotrienes and fatty acids.

60 nding on the modulatory action of harmane on monoamine levels and could potentially be of therapeutic

61 e hypothesis that venlafaxine perturbs brain monoamine levels and disrupts molecular responses essent

62 discrimination problems and examined whether monoamine levels in the orbitofrontal cortex, caudate nu

63 arbolines including harmane modulate central monoamine levels partly through monoamine oxidase (MAO)

64 ver, TPH2 expression and activity as well as monoamine levels were unchanged in the projection areas

65 ce attractor stability, whereas high frontal monoamine levels would severely diminish it.

66 In contrast, d-amphetamine increases brain monoamines' levels, and evokes hyperactivity and anxiety

67 crystal structures of LeuBAT, an engineered monoamine-like version of the bacterial amino acid trans

68 mpared intra-PFC opioid manipulations with a monoamine manipulation (d-amphetamine), in two sucrose-r

69 Computational theories propose that monoamines may exert bidirectional (concentration-depend

70 These results indicate both low monoamine metabolism and neuronal membrane dysfunction a

71 ed a genome-wide association study (GWAS) of monoamine metabolite (MM) levels in cerebrospinal fluid

72 ramine (4-hydroxyphenethylamine), which is a monoamine metabolized by monoamine oxidase (MAO), exists

73 es dopamine (DA) and serotonin (5HT) and the monoamine-metabolizing enzyme monoamine oxidase A (MAOA)

74 macologic profile that combines dose-related monoamine modulation with phosphorylation of intracellul

75 it distinct topological properties, with the monoamine network displaying a highly disassortative sta

76 ion in embryonic mid-hindbrain regions where monoamine neurons emerge.

77 nd encodes a receptor (TAAR1) that modulates monoamine neurotransmission and at which MA serves as an

78 of alpha-synuclein, including modulation of monoamine neurotransmission.

79 drobiopterin (THB), an essential cofactor in monoamine neurotransmitter biosynthesis.

80 t currently available antidepressants target monoamine neurotransmitter function.

81 We provide evidence that a monoamine neurotransmitter may have played a role in the

82 -pituitary-adrenal (HPA) axis dysregulation, monoamine neurotransmitter metabolism, and limbic system

83 Dopamine (DA) is a monoamine neurotransmitter responsible for regulating a

84 regulates neurotransmission by the biogenic monoamine neurotransmitter serotonin (5-HT, 5-hydroxytry

85 termination of ultra-trace concentrations of monoamine neurotransmitter such as noradrenaline (NA) in

86 lase (AADC) deficiency is an inborn error of monoamine neurotransmitter synthesis, which results in d

87 tetrahydrobiopterin, a critical cofactor for monoamine neurotransmitter synthesis.

88 (MAOA), a mitochondrial enzyme that degrades monoamine neurotransmitters and dietary amines.

89 MAOA), a mitochondria-bound enzyme, degrades monoamine neurotransmitters and dietary monoamines.

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 creased white matter and increased levels of monoamine neurotransmitters in the cerebral cortex.

96 Modulation of neural activity by monoamine neurotransmitters is thought to play an essent

97 The covalent agonists are derived from the monoamine neurotransmitters noradrenaline, dopamine, ser

98 Monoamine neurotransmitters such as serotonin, dopamine,

99 othesis that genomic regions associated with monoamine neurotransmitters would be highly differentiat

100 in-binding site of SULT1A3, which sulfonates monoamine neurotransmitters, is modeled on that of 1A1 a

101 icular storage and exocytotic release of all monoamine neurotransmitters.

102 cus coeruleus (LC) and dorsal raphe (DR) are monoamine nuclei implicated in stress-related disorders.

103 f aversive stimuli and inhibitory control of monoamine nuclei.

104 uction protein that controls the function of monoamine, opiate, muscarinic, and other G protein-coupl

105 s nearly doubled and inhibition of firing by monoamines or ML297 was lost.

106 ly demonstrated direct evidence of increased monoamine oxidase (MAO) activity in the brain of a simia

107 tonin 5-HT1A receptor antagonist) as well as monoamine oxidase (MAO) and functional binding assays we

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 The flavoenzyme monoamine oxidase (MAO) regulates mammalian behavioral p

113 lamine), which is a monoamine metabolized by monoamine oxidase (MAO), exists widely in plants, animal

114 ein, a novel one-pot omega-transaminase (TA)/monoamine oxidase (MAO-N) cascade process for the synthe

115 Drug interaction between inhibitors of monoamine oxidase (MAOIs) and selective serotonin (5-hyd

116 However, it has been reported that monoamine oxidase A (MAO A, a major neurotransmitter-deg

117 Monoamine oxidase A (MAO-A) is an important brain enzyme

118 Monoamine oxidase A (MAO-A) is an important enzyme on th

119 o counter the effects of the 40% increase in monoamine oxidase A (MAO-A) levels that occurs during PP

120 One such biological abnormality is elevated monoamine oxidase A (MAO-A) levels, which occurs in the

121 A functional promoter polymorphism in the monoamine oxidase A (MAOA) gene has been implicated as a

122 esonance imaging and genetic analysis of the monoamine oxidase A (MAOA) gene, we investigated how str

123 (5HT) and the monoamine-metabolizing enzyme monoamine oxidase A (MAOA) have been repeatedly implicat

124 We report that monoamine oxidase A (MAOA) is a clinically and functiona

125 Monoamine oxidase A (MAOA) is a mitochondrial enzyme tha

126 The rs1137070 polymorphism of monoamine oxidase A (MAOA) is associated with alcoholism

127 ohorts of Finnish prisoners, revealed that a monoamine oxidase A (MAOA) low-activity genotype (contri

128 Pharmacologic blockade of monoamine oxidase A (MAOA) or serotonin transporter (5-H

129 g growth differentiation factor-3 (GDF3) and monoamine oxidase A (MAOA) that is known to degrade nora

130 6 member 2 (SLC6A2), an NE transporter, and monoamine oxidase A (MAOA), a degradation enzyme.

131 Monoamine oxidase A (MAOA), a mitochondria-bound enzyme,

132 cancer (PCa) exhibit increased expression of monoamine oxidase A (MAOA), a mitochondrial enzyme that

133 rine secretion; P < 0.01), with no effect on monoamine oxidase A (serotonin catabolism), serotonin re

134 NIRKO mice also exhibit increased levels of monoamine oxidase A and B (MAO A and B) leading to incre

135 In a screening for potential monoamine oxidase A and B inhibition ciproxifan showed e

136 ted high selectivity (>160x) against related monoamine oxidase A and B.

137 form (sVAP-1) accounts for most circulating monoamine oxidase activity, has insulin-like effects, an

138 o competitive MPP(+)-dependent inhibition of monoamine oxidase activity.

139 (AD), i.e., acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), a series of multitarget lig

140 A set of drugs was further studied in monoamine oxidase B (MAO-B) and cyclooxygenase-1 (COX-1)

141 l) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10

142 enosine receptors (A2AARs) and inhibition of monoamine oxidase B (MAO-B) in the brain are considered

143 e, competitive, and reversible inhibitors of monoamine oxidase B (MAO-B).

144 was found to suppress the gene expression of monoamine oxidase B (MAOB) in the brain of wild-type but

145 tural comparisons with human metabolites and monoamine oxidase B (MAOB) was identified as the putativ

146 g agent, flecainide, which has no recognized monoamine oxidase B activity, and which has previously b

147 example of a biorelevant synthetic model for monoamine oxidase B activity.

148 onoamine oxidases with slight preference for monoamine oxidase B in both species.

149 We report the effects of the addition of a monoamine oxidase B inhibitor, rasagiline, to antidepres

150 est placebo-controlled clinical trial of the monoamine oxidase B inhibitor, rasagiline, we examined h

151 2D6 inhibitor, quinidine, and also partly by monoamine oxidase B inhibitors deprenyl and pargyline.

152 his, a number of highly potent and selective monoamine oxidase B inhibitors were identified.

153 dowed with potent, selective, and reversible monoamine oxidase B inhibitory activity is a clinically

154 Accordingly, monoamine oxidase blockers pargyline and l-deprenyl had

155 mine (2, MBA236) as a new cholinesterase and monoamine oxidase dual inhibitor.

156 Myelosuppression and monoamine oxidase inhibition (MAOI) are key independent

157 dose response experiments with tricyclic or monoamine oxidase inhibitor antidepressants.

158 While tricyclic and monoamine oxidase inhibitor medications were associated

159 n by RNAi in human erythroid cells or by the monoamine oxidase inhibitor tranylcypromine in human ery

160 covery of a new class of compounds acting as monoamine oxidase inhibitors (MAO-Is) and bearing a 6'-s

161 ects on outcomes compared with waitlist were monoamine oxidase inhibitors (SMD -1.01, 95% credible in

162 idepressants (eg, tricyclic antidepressants, monoamine oxidase inhibitors) were excluded.

163 reated with beta-blockers, ACE inhibitors or monoamine oxidase inhibitors, in children under 5 years

164 etic modeling suggests a lower potential for monoamine oxidase interaction, and animal and human subj

165 The monoamine oxidase isoenzymes (MAOs) A and B play importa

166 es was synthesized and screened toward human monoamine oxidase isoforms (hMAO-A and hMAO-B).

167 The flavin-dependent monoamine oxidase LSD1 (lysine-specific demethylase 1, a

168 g sites for [(18)F]AV-1451, such as neuronal monoamine oxidase or neuromelanin.

169 re, we demonstrate that AMX-2 is the primary monoamine oxidase that metabolizes 5-HT in C. elegans, a

170 e carbidopa/levodopa, dopamine agonists, and monoamine oxidase type B (MAO-B) inhibitors.

171 ptom, aged <60 years) other medications (eg, monoamine oxidase type B inhibitors [MAOBIs], amantadine

172 evelopment and application of a "toolbox" of monoamine oxidase variants from Aspergillus niger (MAO-N

173 cascade consisting of the ATHase, the GDH, a monoamine oxidase, and a catalase leads to the productio

174 d by the transaminase is not affected by the monoamine oxidase, and highlights the potential of this

175 ine oxidase, copper containing 3), a surface monoamine oxidase, as a new marker of myofibroblasts by

176 tabolism of dopamine involves three enzymes: monoamine oxidase, catechol O-methyltransferase, and sul

177 ethyl transferase (COMT) and two isoforms of monoamine oxidase--modulated degree of belief learning a

178 ompanied by an increase in the expression of monoamine oxidase-A (MAO-A) and MAO-B in the lateral OFC

179 Monoamine oxidase-A (MAO-A) is a treatment target in neu

180 study examined how the mitochondrial enzyme monoamine oxidase-A (MAO-A), which produces hydrogen per

181 eas was similarly modulated by inhibition of monoamine oxidase-A and was reduced in animals with indu

182 -serotonin and increased after inhibition of monoamine oxidase-A, the main enzyme responsible for ser

183 oduce the inhibitory gliotransmitter GABA by monoamine oxidase-B (Maob) and abnormally release GABA t

184 arins were designed, prepared, and tested as monoamine oxidases (MAOs) and acetyl- and butyryl-cholin

185 carbonyl reductases (CREDs), hydrolases and monoamine oxidases (MAOs), providing a comprehensive ove

186 Monoamine oxidases A and B (MAO-A and MAO-B) are enzymes

187 cture (which also has inhibitory activity at monoamine oxidases A and B and at the serotonin and nore

188 ty towards acetyl/butyrylcholinesterases and monoamine oxidases A/B as well as the histamine H3 recep

189 As the H3R and monoamine oxidases are all capable of affecting neurotra

190 M1 family is homologous to the mitochondrial monoamine oxidases MAO-A/B and produces hydrogen peroxid

191 omolar concentration range for human and rat monoamine oxidases with slight preference for monoamine

192 and tested for inhibitory activities against monoamine oxidases.

193 terases, N-methyl-D-aspartate receptors, and monoamine oxidases.

194 Antidepressants elevate concentrations of monoamines, particularly serotonin, but it remains uncer

195 Mutations affecting single monoamine pathways did not affect reserpine sensitivity,

196 PPB, a dietary supplement kit consisting of monoamine precursor amino acids and dietary antioxidants

197 This monoamine-receptor activity causes pericytes to locally

198 oxia owing to paradoxical excess activity of monoamine receptors (5-HT1) on pericytes, despite the ab

199 ervated by monoamines, and drugs that target monoamine receptors have been used to treat a number of

200 Inhibition of monoamine receptors or of AADC, or even an increase in i

201 Non-classical monoamine recognition evolved in two steps: an ancestral

202 aggression, but a mechanistic account of how monoamines regulate antisocial motives remains elusive.

203 inhibitor (via the parent drug PDM) and as a monoamine releaser (via the active metabolite PM).

204 ylenedioxymethamphetamine (MDMA) is a potent monoamine releaser that produces an acute euphoria in mo

205 MDMA, a potent monoamine-releaser with particularly pronounced serotoni

206 Receptor activation in the absence of monoamines results from the production of trace amines (

207 dosing with dasotraline, a long-acting, dual monoamine reuptake inhibitor, may be a safe and efficaci

208 s site of action in blocking the function of monoamine reuptake transporters, increasing synaptic lev

209 Monoamine serotonin (5HT) has been linked to aggression

210 The membrane transporters for the monoamines serotonin (SERT) and dopamine (DAT) are promi

211 nduced by brainstem neurons that release the monoamines serotonin and noradrenaline, and local vessel

212 developmental periods that are sensitive to monoamine signaling and impact adult behaviors of releva

213 Here we test the hypothesis that increased monoamine signaling during development causes these para

214 nction as a consequence of increased P22-P41 monoamine signaling might underlie altered aggression.

215 data show that VMAT1 polymorphisms influence monoamine signaling, the functional response of emotiona

216 icinus lipocalins have the potential to bind monoamines similar to other tick species previously repo

217 The clinically safe monoamine stabilizer (-)-OSU6162 (OSU6162) restores dopa

218 s in specific defects in peptide hormone and monoamine storage and regulated secretion.

219 heir cognate substrates and sustain cellular monoamine stores even during neuronal activity.

220 al fluid-contacting (CSF-c) cells containing monoamines such as dopamine (DA) and serotonin (5-HT) oc

221 tion of hindbrain patterning genes can alter monoamine system development and thereby produce forebra

222 The monoamine system in the prefrontal cortex has been impli

223 neuropsychiatric disorders, we characterized monoamine systems in relation to forebrain neurogenesis

224 lsivity and motivation relative to PFC-based monoamine systems.

225 ndard antidepressant medications that target monoamine systems.

226 ress, facilitates apoptosis, and metabolizes monoamines, therapeutics opposing these processes are pr

227 SLC18A2 is involved in transporting monoamines to synaptic vesicles and has been implicated

228 amily of transporters, mediates transport of monoamines to synaptic vesicles and storage organelles i

229 These hypotheses include disruptions in monoamine transmission, hypothalamus-pituitary-adrenal a

230 the effort-related effects of the vesicular monoamine transport (VMAT-2) inhibitor tetrabenazine (TB

231 iduals with BPD and leads to marked increase monoamine transport in vitro.

232 t cell clusters incubated with the vesicular monoamine transport inhibitor, reserpine.

233 reduced after acute treatment with vesicular monoamine transport inhibitors or selective destruction

234 ro, with the Ile allele leading to increased monoamine transport into presynaptic vesicles.

235 ization of one of them, Brevibacillus brevis monoamine transporter (BbMAT), from the bacterium B. bre

236 used a mutation in the Drosophila vesicular monoamine transporter (dVMAT) as a sensitized genetic ba

237 afficking domain of the Drosophila vesicular monoamine transporter (DVMAT), which is required for the

238 cation 3 transporter (OCT3)/plasma membrane monoamine transporter (PMAT) inhibitor, increased the 5-

239 ed bacterial homologues of the rat vesicular monoamine transporter (rVMAT2).

240 pharmacological inhibition of the vesicular monoamine transporter (VMAT) blocks amphetamine-induced

241 oited the broad requirement of the vesicular monoamine transporter (VMAT) for the vesicular storage a

242 Overexpression of the vesicular monoamine transporter (VMAT) rescued the dopamine toxici

243 a small-molecule inhibitor of the vesicular monoamine transporter (VMAT) that repackages monoamines

244 Vesicular monoamine transporter (VMAT), a member of the largest su

245 hloroamphetamine (pCA), acting via vesicular monoamine transporter (VMAT), and a charged VMAT, substr

246 continuous pumping activity of the vesicular monoamine transporter (VMAT)2.

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 Vesicular monoamine transporter 2 (VMAT2) catalyzes transport of m

251 We previously reported that the vesicular monoamine transporter 2 (VMAT2) is physically and functi

252 neurons projecting to the LHb lack vesicular monoamine transporter 2 (VMAT2) mRNA, and there is littl

253 e neurotransmitter 200 (FFN200), a vesicular monoamine transporter 2 (VMAT2) substrate that selective

254 for the serotonin transporter and vesicular monoamine transporter 2 (VMAT2).

255 AC)-mediated overexpression of the vesicular monoamine transporter 2 (VMAT2; Slc18a2).

256 mutation in SLC18A2 (which encodes vesicular monoamine transporter 2 [VMAT2]).

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 TH(+) cells expressed both VMAT2 (vesicular monoamine transporter 2) and VGAT (vesicular GABA transp

260 o (OR)=1.4, p=2.1E-05) in SLC18A2 (vesicular monoamine transporter 2).

261 omography (PET) radioligand to the vesicular monoamine transporter 2, (VMAT2), [(11)C]dihydrotetraben

262 d genes tyrosine hydroxylase (TH), vesicular monoamine transporter 2, dopamine transporter and aldehy

263 cular acetylcholine transporter or vesicular monoamine transporter 2.

264 an antidepressive agent and a non-selective monoamine transporter inhibitor that blocks the reuptake

265 ethylenedioxyamphetamine analogs bind at the monoamine transporter orthosteric binding site by adopti

266 requires metabolism to the amphetamine-like monoamine transporter substrate phenmetrazine (PM) to pr

267 on of decarboxylase activity (FD), vesicular monoamine transporter type 2 (DTBZ), and dopamine transp

268 Vesicular monoamine transporter type 2 (VMAT2) imaging with PET al

269 ([(11)C]DTBZ) binding to striatal vesicular monoamine transporter type 2 (VMAT2) in cocaine abusers

270 BZ), a novel radiotracer targeting vesicular monoamine transporter type 2 (VMAT2), has been proven as

271 toradiographic measures of DAT and vesicular monoamine transporter type 2 (VMAT2), striatal dopamine,

272 demonstrated that the reduction of vesicular monoamine transporter type 2 availability was obviously

273 The mean reductions of vesicular monoamine transporter type 2 density for the caudate, pu

274 hydrotetrabenazine (DTBZ; reflects vesicular monoamine transporter type 2), ex vivo quantification of

275 ministration of the VMAT-2 (type-2 vesicular monoamine transporter) inhibitor tetrabenazine (9,10-dim

276 ficient relay between SERT and the vesicular monoamine transporter-2 (VMAT2).

277 Furthermore, DAT and vesicular monoamine transporter-2 expressions were similar in the

278 doses of deutetrabenazine-a novel vesicular monoamine transporter-2 inhibitor-in patients with tardi

279 rboxylase, the DA transporter, and vesicular monoamine transporter-2 with EGFP in midbrain dopaminerg

280 tion transporters (OCTs) and plasma membrane monoamine transporter], which may limit the ability of S

281 in receptors (e.g., serotonin receptors) and monoamine transporters (i.e., serotonin, dopamine, and n

282 at the extracellular thin gate is present in monoamine transporters and that a dynamic interaction is

283 pports the concept that uptake and efflux at monoamine transporters are asymmetric processes that can

284 C, and HHMC were substrate-type releasers at monoamine transporters as determined in vitro, but only

285 The plasmalemmal monoamine transporters clear the extracellular space fro

286 loiting structural templates known to target monoamine transporters for dopamine, norepinephrine, and

287 Dysregulation of ion movement through monoamine transporters has been shown to impact neuronal

288 esults provide new insights into the role of monoamine transporters in autophagy regulation and ident

289 nal activities of the compounds at all three monoamine transporters in native brain tissue and cells

290 that define substrates and inhibitors at the monoamine transporters is critical to elucidating the me

291 The serotonin transporter (SERT) and other monoamine transporters operate in either a forward trans

292 ate fast-acting currents, I suggest that the monoamine transporters should be considered as ionotropi

293 ed pore" mechanism in the mammalian synaptic monoamine transporters, and the archaeal GltPh, which is

294 r (LeuT) is a bacterial homolog of the human monoamine transporters, which are important pharmaceutic

295 king mechanism is unique to DAT or common to monoamine transporters.

296 with two clinically relevant compounds: the monoamine uptake inhibitor bupropion and the dopamine an

297 e ability of acute administration of various monoamine uptake inhibitors to reverse the effects of TB

298 use it may simultaneously function as both a monoamine-uptake inhibitor (via the parent drug PDM) and

299 tive action of acetylcholine (ACh), GABA and monoamines, which lead to transitions between primary br

300 rocess that involves exchange of the charged monoamine with two protons.