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1 hols (dopamine, epinephrine, norepinephrine, 3, 4-dihydroxyphenylacetic acid.
3 etaldehyde, a potentially toxic aldehyde, to 3,4-dihydroxyphenylacetic acid, a non toxic metabolite.
4 ine (DA) and serotonin and their metabolites 3,4-dihydroxyphenylacetic acid and 5-hydroxyindole aceti
5 omatic L-amino acid decarboxylase, dopamine, 3,4-dihydroxyphenylacetic acid and homovanillic acid wer
6 d by a decrease in the dopamine metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid, as
7 lues reflect rates of dopamine metabolism to 3,4-dihydroxyphenylacetic acid and homovanillic acid, ou
8 r 3,4-dihydroxyphenylalanine, and metabolite 3,4-dihydroxyphenylacetic acid completely block the nitr
9 rease in the concentration of dopamine (DA), 3, 4-dihydroxyphenylacetic acid (DOPAC), and homovanilli
10 oncentrations of DA and its main metabolite, 3, 4-dihydroxyphenylacetic acid (DOPAC), in the median e
11 for MAO A, but not MAO B, and the levels of 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyra
12 significant increase in both DA metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic
13 sal concentrations of DA or its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic
14 ellular levels of DA and the DA metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic
15 pletion of dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic
16 exhibited by a loss of DA and DA metabolite [3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic
17 20 min after injection while DA metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic
18 leus accumbens, and an increase in dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and serotonin.
19 ed extracellular levels of dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) at all doses and
21 tially affects basal and evoked dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) content in the su
22 f 5-hydroxyindole-3-acetic acid (5-HIAA) and 3,4-dihydroxyphenylacetic acid (DOPAC) from their respec
23 , 5-hydroxyindole-3-acetic acid (5-HIAA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in isolated hamst
24 ntification of DA and its primary metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in mouse retina.
25 ring the concentrations of the DA metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the median emi
28 ole increased concentrations of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) in the paraventri
29 The effects of the synthesized compounds on 3,4-dihydroxyphenylacetic acid (DOPAC) levels correlated
30 ortionally greater depletion of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) levels in the str
31 f DA metabolites homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) reflected changes
33 of oxidation products of dopamine, DOPA, and 3,4-dihydroxyphenylacetic acid (DOPAC) to inhibit protea
34 tent of dopamine and the dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) were measured by
35 nhibition) and metabolism (concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC)) in terminals of
36 taneously to assess changes in ascorbate and 3,4-dihydroxyphenylacetic acid (DOPAC), a major dopamine
37 ere that substoichiometric concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC), a normal product
38 extracellular basal levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), and 4-hydroxy-3-
39 bens (NAS), ethanol decreased dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), and HVA levels i
40 eased levels of dopamine and its metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), as well as serot
41 hrine, 3,4-dihydroxy-phenylalanine (L-DOPA), 3,4-dihydroxyphenylacetic acid (DOPAC), methyldopamine,
46 nificant increase in the levels of dopamine, 3-4-dihydroxyphenylacetic acid (DOPAC) and homovanillic
47 (DA concentrations) and catabolic activity (3,4-dihydroxyphenylacetic acid; DOPAC) of A11 DA neurons
48 ll as metabolites 5-hydroxyindolacetic acid, 3,4-dihydroxyphenylacetic acid, homovanillic acid, and 3
49 riatum and enhanced levels of the metabolite 3,4-dihydroxyphenylacetic acid in frontal cortex and hyp
50 significantly reduced levels of dopamine and 3,4-Dihydroxyphenylacetic acid in the striatum as well a
51 also characterized, including ascorbic acid, 3,4-dihydroxyphenylacetic acid, serotonin, adenosine, an
52 HT should previously be oxidized to DOPAC (3,4-dihydroxyphenylacetic acid) which reacts with MGO by
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