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1                                              DOPAC and HVA changes were measured at 1 day and were re
2                                              DOPAC and norepinephrine concentrations were determined
3                                              DOPAC concentrations were significantly lower in caudate
4                                              DOPAC levels remained stable, arguing against an AAO-ind
5                                              DOPAC levels significantly increased in adults after 15
6                                              DOPAC was detected as the major degradation product of H
7                                              DOPAC was used as an index of dopaminergic activity.
8                                              DOPAC/DA ratio, an indicator of dopaminergic neuronal ac
9 tabolite 18F-dihydroxyphenylacetic acid (18F-DOPAC).
10 e ratio of myocardial 18F-DA to arterial 18F-DOPAC provided an index of vesicular uptake.
11 ne (NE) and 3,4-dihydroxyphenyl-acetic acid (DOPAC) in the brain frontal cortex were measured in 20-m
12 to the presence of 3,4-dihydroxyacetic acid (DOPAC) in the brain extracellular fluid.
13 he levels of 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyramine (3-MT) in the striatum.
14 of dopamine, 3-4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) and in the DOPAC/dopa
15  metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in caudate nucleus re
16 metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), were elevated over t
17 metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), were found to be dec
18 metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA).
19 metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA).
20  metabolite [3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA)] levels and tyrosine
21 in dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and serotonin.
22 ine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) at all doses and the serotonin (5-HT) metabolite,
23  oxidized to 3,4-dihydroxyphenylacetic acid (DOPAC) by aldehyde dehydrogenase (ALDH), but is also par
24  striatal DA and dihydroxyphenylacetic acid (DOPAC) concentrations were determined for the lesioned a
25  of dopamine and dihydroxyphenylacetic acid (DOPAC) concentrations were determined from the 6-OHDA le
26 dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) content in the subareas of the neostriatum and nu
27 (5-HIAA) and 3,4-dihydroxyphenylacetic acid (DOPAC) from their respective amines in isolated mitochon
28 ycol (DHPG), and dihydroxyphenylacetic acid (DOPAC) in hypothalamic paraventricular nucleus (PVN) mic
29 (5-HIAA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in isolated hamster or rat liver mitochondria.
30 y metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in mouse retina.
31 opamine (DA) and dihydroxyphenylacetic acid (DOPAC) in striatum and nucleus accumbens than susceptibl
32 on of DA and 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence (ME) and various regions o
33 on of DA and 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence (ME), as well as the anter
34 A metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence which contains terminals o
35 dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) in the paraventricular nucleus (PVN) of the hypot
36 compounds on 3,4-dihydroxyphenylacetic acid (DOPAC) levels correlated very well with their affinity f
37 dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) levels in the striatum, and a greater increase in
38 id (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) reflected changes in tissue DA concentrations, in
39 nd ascorbate and dihydroxyphenylacetic acid (DOPAC) rejection at the overoxidized polypyrrole-coated
40 estraint stress, dihydroxyphenylacetic acid (DOPAC) to DA ratios in the mPfx, NAs and ST increased in
41 the ratio of 3,4-dihydroxyphenylacetic acid (DOPAC) to DA.
42 e, DOPA, and 3,4-dihydroxyphenylacetic acid (DOPAC) to inhibit proteasomal activity.
43 d the metabolite dihydroxyphenylacetic acid (DOPAC) were elevated (by 98% and 65%, respectively) in t
44 e metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) were measured by HPLC with electrochemical detect
45 levels of DA and dihydroxyphenylacetic acid (DOPAC) were not different in striata collected from mela
46 ntrations of 3,4-dihydroxyphenylacetic acid (DOPAC)) in terminals of these neurons in the median emin
47 scorbate and 3,4-dihydroxyphenylacetic acid (DOPAC), a major dopamine metabolite, near the infusion s
48 ntrations of 3,4-dihydroxyphenylacetic acid (DOPAC), a normal product of the metabolism of dopamine,
49 pamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), and 4-hydroxy-3-methoxyphenylacetic acid (HVA) w
50 amine (DA), 3, 4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) by 76%, 53% and 40%,
51 pamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), and HVA levels in rats that exhibited low levels
52  metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), as well as serotonin and 5-hydroxyindole acetic
53 r dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxyindoleacetic a
54 c acid (HVA) and dihydroxyphenylacetic acid (DOPAC), in five brain regions from suicide victims with
55 metabolite, 3, 4-dihydroxyphenylacetic acid (DOPAC), in the median eminence and the three pituitary l
56 ne (L-DOPA), 3,4-dihydroxyphenylacetic acid (DOPAC), methyldopamine, and tyramine, which gave negligi
57 sulphate and 3,4-dihydroxyphenylacetic acid (DOPAC)-sulphate were the main metabolites, followed by D
58 dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC).
59 bic acid and 3,4-dihydroxyphenylacetic acid (DOPAC).
60 ar levels of 3,4-dihydroxyphenylacetic acid (DOPAC).
61 ts metabolite dihydroxy-O-phenylacetic acid (DOPAC) were extracted from medial prefrontal cortex (mPF
62 ltering discriminated against ascorbic acid, DOPAC, and acidic pH changes, three common interferences
63 found in the brain, including ascorbic acid, DOPAC, and serotonin.
64 ic activity (3,4-dihydroxyphenylacetic acid; DOPAC) of A11 DA neurons innervating the lumbar spinal c
65 re was no sexual difference in the activity (DOPAC/DA ratio) of these DA neurons under basal conditio
66 y transmission, light exposure did not alter DOPAC levels in the nob mice.
67                                    Although, DOPAC decreased in both groups following AMPH injection,
68 attenuation of the response to ascorbate and DOPAC, common interferences of dopamine in vivo.
69                 Internal standards DA-d4 and DOPAC-d5 result in standard curve linearity for DA from
70                     Concentrations of DA and DOPAC from tissues and the concentration of PRL in plasm
71 re dissected and the concentration of DA and DOPAC in each was measured by HPLC-EC.
72  examined the effect of anesthesia on DA and DOPAC levels in the retina in vivo and find that basal d
73 al dopaminergic tone (i.e.: increased DA and DOPAC levels) and improves behavioral performance (i.e.:
74                    When combining the DA and DOPAC measures from these two experiments, the data sugg
75 re no changes in the concentration of DA and DOPAC of the IL due to the suckling stimulus.
76 , a decrease in the concentrations of DA and DOPAC was detected in the inner zone of the AL (AL-IZ).
77 nimals, basal extracellular levels of DA and DOPAC were significantly decreased in two groups of aged
78 icantly reduced striatal TH activity, DA and DOPAC, but there were no significant differences in the
79 ficantly alter the striatal levels of DA and DOPAC, while it slightly reduced HVA concentration.
80 n combination, on striatal dopamine (DA) and DOPAC levels, and the density of tyrosine hydroxylase (T
81 levels were not significantly decreased, and DOPAC and HVA levels were decreased by only 65% and 30%,
82 .8-fold and PVN microdialysate NE, DHPG, and DOPAC by 1.2, 0.6 and 0.5-fold.
83 O on plasma and microdialysate NE, DHPG, and DOPAC.
84 ine (EPI), DHPG, dihydroxyphenylalanine, and DOPAC levels by 4.3, 7.3, 2.5, 0.6 and 1.8-fold and PVN
85     Elevated cysteinyl adducts to L-DOPA and DOPAC are seen early and are followed by increased stria
86                          Dopamine, DOPA, and DOPAC underwent tyrosinase-catalyzed oxidation to genera
87 nt reduction in corpus striatal dopamine and DOPAC but not norepinephrine.
88 duced striatal reduced striatal dopamine and DOPAC concentrations, regardless of hormonal condition o
89  alone failed to alter striatal dopamine and DOPAC concentrations, with levels obtained being similar
90 mphetamine-induced depletion of dopamine and DOPAC in red wine treated mice.
91 uced a significant depletion of dopamine and DOPAC in the striatum.
92 dependent reduction of striatal dopamine and DOPAC levels but did not alter HVA, 5-HT, or 5-HIAA.
93                                 Dopamine and DOPAC levels in striatal tissue were analyzed using HPLC
94                        However, dopamine and DOPAC levels were significantly lower in the nob mice co
95 rvival, and striatal and nigral dopamine and DOPAC levels, were evaluated 2 weeks after the lesions.
96 ereotypy, and nucleus accumbens dopamine and DOPAC release responses to an injection of saline follow
97  led to a reduction of striatal dopamine and DOPAC that were both non-significantly greater than that
98 L concentrations while diminishing DOPET and DOPAC levels.
99 mster ethanol intake also inhibit 5-HIAA and DOPAC formation.
100 significant increases in the 5-HIAA/5-HT and DOPAC/DA ratios, often used as measures of turnover.
101 tion, DA was not altered but DOPAC level and DOPAC/DA turnover ratios were significantly reduced.
102 ssue DA levels, but reduced DOPAC levels and DOPAC/DA ratios.
103 the increase in the DOPAC and HVA levels and DOPAC/dopamine ratio induced by L-DOPA in the substantia
104  while the striatal DOPAC and HVA levels and DOPAC/dopamine ratio were significantly reduced as compa
105 r DA from 0.05-100 ng/mL (LOD = 6 pg/mL) and DOPAC from 0.5-100 ng/mL (LOD = 162 pg/mL).
106  of other catecholamine derivatives, such as DOPAC and 3,4-dihydroxyphenylethyleneglycol.
107 er mTBI or injection, DA was not altered but DOPAC level and DOPAC/DA turnover ratios were significan
108 phate were the main metabolites, followed by DOPAC and homovanillic acid (HVA).
109  epinephrine (Epi) or monoamine catabolites (DOPAC, 5-HIAA) at any ammonia concentrations tested.
110            One striatum was examined for DA, DOPAC, and HVA levels using HPLC-EC and the contralatera
111 gdala and hippocampus, and dopamine (HVA/DA, DOPAC/DA) in prefrontal cortex.
112 al cortex of adult rats, basal levels of DA, DOPAC and HVA did not differ across prenatal treatments;
113 TH-induced hyperthermia and depletion of DA, DOPAC and HVA.
114 ysis revealed a significant depletion of DA, DOPAC, and HVA at all time points.
115            In the adult, basal levels of DA, DOPAC, HVA and 5-HIAA in n. accumbens did not differ acr
116                  NDN activity, defined by DA:DOPAC ratio in nerve terminals, was determined by HPLC-E
117 th estrogen had the opposite effect of DHTP, DOPAC/DA and MHPG/NE ratios increased to a greater level
118 its metabolites, 3,4-dihydroxyphenylalanine (DOPAC) and homovanillic acid (HVA); norepinephrine (NE)
119 sine hydroxylase-immunoreactivity, dopamine, DOPAC, and serotonin than wild-type mice.
120 ridone on ex vivo tissue levels of dopamine, DOPAC, HVA, 5-HT and 5-HIAA in multiple brain regions.
121  (at 6 and 12 h) increase in median eminence DOPAC concentrations in these animals which was blocked
122  administration of PRL-AB on median eminence DOPAC concentrations suggesting that the tonic stimulato
123 olactinemia) failed to alter median eminence DOPAC concentrations unless prolactin exposure was reins
124 ion of mRNA encoding TH and DAT, and enteric DOPAC (the specific dopamine metabolite).
125 ere accompanied by declines in extracellular DOPAC concentrations, and these declines were the same 2
126 haloperidol exposure increased extracellular DOPAC, and this haloperidol-stimulated DOPAC increase wa
127                 Measurement of extracellular DOPAC, a dopamine metabolite, following l-DOPA injection
128 uenced the effect of D-AMPH on extracellular DOPAC, as the D-AMPH-related decreases in DOPAC were gre
129                              HT-glucuronide, DOPAC-glucuronide, HVA-glucuronide and HVA-sulphate were
130 e compounds with 1,2-dihydroxyphenyl groups (DOPAC and catechol), their 1,4-dihydroxyphenyl isomers (
131 se in DA turnover, as indicated by a higher (DOPAC+HVA)/DA ratio, seems to be associated to rotenone-
132  at the lowest dose of risperidone; however, DOPAC showed a dose dependent increase.
133                              24 h after IBO, DOPAC concentrations in striatum and HVA levels in the f
134  by DNQX was not associated with a change in DOPAC/DA level in the nucleus accumbens or the striatum.
135 on of striatal DA (as measured by changes in DOPAC) may be altered.
136 e catabolism (as assessed by the decrease in DOPAC and HVA levels) in the striatum and substantia nig
137  was accompanied by a pronounced decrease in DOPAC concentrations in the median eminence of females,
138 PAC in the median eminence and a decrease in DOPAC in the nucleus accumbens; surgical deafferentation
139 ar DOPAC, as the D-AMPH-related decreases in DOPAC were greater for a concentration when it was admin
140 trast to that of dopamine, no differences in DOPAC concentrations between estrogen and non-estrogen-t
141 nelorane caused a dose-dependent increase in DOPAC in the median eminence and a decrease in DOPAC in
142           Light caused a similar increase in DOPAC/DA ratio but interindividual variation was signifi
143 prevented the open field induced increase in DOPAC/DA, MHPG/NE, and 5-HIAA/5-HT ratio.
144 increases were characterized by increases in DOPAC, HVA, MHPG and 5-HIAA coupled with decreases in DA
145 ced an increase in DA utilization (increased DOPAC/DA ratio) in mPFC and NAS, but not striatum.
146                                        Lower DOPAC concentrations were largely restricted to those su
147 e CSF measured higher levels of DA and lower DOPAC/DA ratios among the heavy drinkers at the same tim
148 found a reduction in the dopamine metabolite DOPAC in the striatum of these mice.
149 w levels of dopamine (DA) and its metabolite DOPAC.
150 centrations of DA and its primary metabolite DOPAC were determined by high-performance liquid chromat
151 re was an increase in a dopamine metabolite, DOPAC and histologically, DA axons in the striatum were
152 iatal content of dopamine or its metabolite, DOPAC.
153 lar levels of dopamine, dopamine metabolites DOPAC and HVA, and the major 5-HT metabolite 5-HIAA, in
154 ochemical analyses of DA and its metabolites DOPAC and HVA show that exercise also functionally prote
155 t depletion of dopamine, and its metabolites DOPAC and HVA, as well as the significant formation of 3
156 ls of striatal dopamine and its metabolites (DOPAC and HVA) following MPTP treatment as determined by
157 ults; however, the levels of DA metabolites, DOPAC, HVA, and the serotonin metabolite, 5-HIAA, were m
158 e depletion of dopamine and its metabolites, DOPAC and HVA and the formation of 3-NT in PC12 cells.
159  The levels of dopamine and its metabolites, DOPAC and HVA were analyzed by HPLC equipped with electr
160                            In contrast, MPOA DOPAC concentrations did not increase in prepubertal mal
161 ess, 6-OHDA-induced increases in neostriatal DOPAC/DA and HVA/DA ratios were normalized by age/food-d
162 of alpha-Syn, due to non-covalent binding of DOPAC to alpha-Syn monomer.
163 n the NL, a decrease in the concentration of DOPAC was detected due to the suckling stimulus.
164                         The concentration of DOPAC was increased in the ME and NL, decreased in the I
165 nt-treated suicides, lower concentrations of DOPAC were observed in the basal ganglia, reaching stati
166 oxidation of DOPAC, and the oxidized form of DOPAC (the quinone) is responsible for the fibrillation
167 of ALDH by daidzein reduced the formation of DOPAC and increased the accumulation of DOPAL.
168 D-AMPH also resulted in diminished levels of DOPAC in the aged rats compared to the young rats.
169  mg/kg s.c.) also increased tissue levels of DOPAC, HVA and 5-HIAA by 169, 221 and 134% of basal leve
170 istration of LY379268, mPFC tissue levels of DOPAC, HVA and 5-HIAA were increased in a dose-dependent
171                                 Oxidation of DOPAC by tyrosinase generated furanoquinone, which was a
172 Syn accelerates the spontaneous oxidation of DOPAC, and the oxidized form of DOPAC (the quinone) is r
173                 In addition, the presence of DOPAC leads to the oxidation of the methionine residues
174 o the H(2)O(2) production as a by-product of DOPAC oxidation.
175 arying estrogen treatments on striatal DA or DOPAC concentrations.
176  In addition, there were no changes of DA or DOPAC in the outer zone of the AL (AL-OZ) due to sucklin
177 r basal tissue concentrations of dopamine or DOPAC or the DOPAC:dopamine ratio in either the nucleus
178  effects on mitochondria-catalyzed 5-HIAA or DOPAC formation and hamster ethanol intake reveals a pos
179 ion-the stronger the inhibition on 5-HIAA or DOPAC formation, the greater the ethanol intake suppress
180  ethanol intake and inhibition of 5-HIAA (or DOPAC) formation by six structural analogues of daidzin
181  suggest that HT and its degradation product DOPAC could have a relevant role in preventing the forma
182     Moreover, both dopamine turnover ratios (DOPAC/DA, HVA/DA) and the serotonin turnover ratio (5-HI
183 mTBI increased tissue DA levels, but reduced DOPAC levels and DOPAC/DA ratios.
184 ed dopamine turnover, as judged from reduced DOPAC levels, in depressed suicides, although we cannot
185         Co-treatment with MA further reduced DOPAC/DA ratios in striatum.
186 lular DOPAC, and this haloperidol-stimulated DOPAC increase was also greatly attenuated at 6 compared
187 droxydopamine-induced reductions in striatal DOPAC levels in all age groups.
188 al dopamine was increased while the striatal DOPAC and HVA levels and DOPAC/dopamine ratio were signi
189 rcle determinations, with the exception that DOPAC levels from Orchidectomized mice were significantl
190 ible explanation for this phenomenon is that DOPAC stabilizes the normally transient oligomers and pr
191  of the alpha-Syn Y39W variant suggests that DOPAC binds non-covalently to the same N-terminal region
192                                          The DOPAC concentrations on the non-lesioned side of the str
193                   The data obtained from the DOPAC determinations imply that this capacity of estroge
194 In animals injected with oPRL at 0900 h, the DOPAC/DA ratio increased in the ME, IL and NL within 1 h
195 bitors also counteracted the increase in the DOPAC and HVA levels and DOPAC/dopamine ratio induced by
196        Although there were no changes in the DOPAC to DA ratio (i.e., turnover), DOPAC levels also fo
197        Moreover, a secondary increase in the DOPAC/DA ratio in the IL and NL occurred during the afte
198 lopride caused a significant increase in the DOPAC/DA ratio in the striatum and nucleus accumbens in
199  mouse retinae a significant increase in the DOPAC/DA ratio is observed following in vivo light stimu
200 OPAC) and homovanillic acid (HVA) and in the DOPAC/dopamine ratio in the putamen, caudate and substan
201  pressure stress significantly increased the DOPAC:dopamine ratio in the nucleus accumbens shell of l
202 e concentrations of dopamine or DOPAC or the DOPAC:dopamine ratio in either the nucleus accumbens cor
203     Co-treatment with MA further reduced the DOPAC/DA ratio.
204 xidative metabolic conversion of dopamine to DOPAC by the mitochondrial enzyme, monoamine oxidase.
205          HT should previously be oxidized to DOPAC (3,4-dihydroxyphenylacetic acid) which reacts with
206 35% postreperfusion increase in DA turnover (DOPAC + HVA/DA) at 5 min after reperfusion.
207 s in the DOPAC to DA ratio (i.e., turnover), DOPAC levels also followed this pattern.
208 both stressed and non-stressed groups, while DOPAC levels were unaffected by treatment group.

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