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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.
8 e area, glial activation, CNS cytokines, and monoamine and amino acid neurotransmitters were quantifi
15 synaptic volume transmission, especially via monoamines and neuropeptides, is also critical to brain
19 S9-2) plays a key modulatory role in opioid, monoamine, and other G-protein-coupled receptor response
22 these studies could potentially affect other monoamines, and the scarcity of imaging evidence on dopa
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
30 predictive of reduced central nervous system monoamines by bioinformatics analyses and confirmed by h
32 (Tph2, SERT, and Pet-1) genes, and midbrain monoamine content in mice raised under control Equinox (
36 nd solitary locusts co-injected by these two monoamines displayed the same tendency as the olfactory
39 ely, it is thought that, with one exception, monoamines (dopamine, serotonin, and norepinephrine) sig
42 erived hypothesis that moderate increases in monoamine efflux would enhance attractor stability, wher
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
48 tered on neurochemical deficits, such as the monoamine hypothesis, research toward this goal has shif
51 ion among their symptoms, the implication of monoamines in depression, and the hypothesis that PrP(C)
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
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
63 mpared intra-PFC opioid manipulations with a monoamine manipulation (d-amphetamine), in two sucrose-r
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
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.
81 regulates neurotransmission by the biogenic monoamine neurotransmitter serotonin (5-HT, 5-hydroxytry
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
86 (MAOA), a mitochondrial enzyme that degrades monoamine neurotransmitters and dietary amines, in strom
89 ng DMT at concentrations comparable to known monoamine neurotransmitters and raise the possibility th
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
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.
103 f aromatic l-amino acids to produce aromatic monoamines or aromatic acetaldehydes, respectively.
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
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
114 lamine), which is a monoamine metabolized by monoamine oxidase (MAO), exists widely in plants, animal
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
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
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
133 cancer (PCa) exhibit increased expression 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
139 form (sVAP-1) accounts for most circulating monoamine oxidase activity, has insulin-like effects, an
141 (AD), i.e., acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), a series of multitarget lig
143 l) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10
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
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
154 dowed with potent, selective, and reversible monoamine oxidase B inhibitory activity is a clinically
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,
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
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
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
185 -serotonin and increased after inhibition of monoamine oxidase-A, the main enzyme responsible for ser
188 arins were designed, prepared, and tested as monoamine oxidases (MAOs) and acetyl- and butyryl-cholin
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
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
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
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
204 that the loss of the kinase may dysregulate monoamine receptors within these neurons, whose activity
206 aggression, but a mechanistic account of how monoamines regulate antisocial motives remains elusive.
208 may mediate pro-social effects by modulating monoamine release in limbic and cortical areas, which wa
210 ylenedioxymethamphetamine (MDMA) is a potent monoamine releaser that produces an acute euphoria in mo
213 dosing with dasotraline, a long-acting, dual monoamine reuptake inhibitor, may be a safe and efficaci
218 nduced by brainstem neurons that release the monoamines serotonin and noradrenaline, and local vessel
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
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
230 neuropsychiatric disorders, we characterized monoamine systems in relation to forebrain neurogenesis
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
236 the effort-related effects of the vesicular monoamine transport (VMAT-2) inhibitor tetrabenazine (TB
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
242 cation 3 transporter (OCT3)/plasma membrane monoamine transporter (PMAT) inhibitor, increased the 5-
244 pharmacological inhibition of the vesicular monoamine transporter (VMAT) blocks amphetamine-induced
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
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
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
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
264 an antidepressive agent and a non-selective monoamine transporter inhibitor that blocks the reuptake
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
270 ([(11)C]DTBZ) binding to striatal vesicular monoamine transporter type 2 (VMAT2) in cocaine abusers
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,
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
280 in receptors (e.g., serotonin receptors) and monoamine transporters (i.e., serotonin, dopamine, and n
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
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
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
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