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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
11 ne (NE) and 3,4-dihydroxyphenyl-acetic acid (DOPAC) in the brain frontal cortex were measured in 20-m
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
20 metabolite [3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA)] levels and tyrosine
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.
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
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
61 pamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC)/DA ratio, and vesicular monoamine transporter 2 (
62 ts metabolite dihydroxy-O-phenylacetic acid (DOPAC) were extracted from medial prefrontal cortex (mPF
63 ltering discriminated against ascorbic acid, DOPAC, and acidic pH changes, three common interferences
65 ic activity (3,4-dihydroxyphenylacetic acid; DOPAC) of A11 DA neurons innervating the lumbar spinal c
66 re was no sexual difference in the activity (DOPAC/DA ratio) of these DA neurons under basal conditio
73 examined the effect of anesthesia on DA and DOPAC levels in the retina in vivo and find that basal d
74 al dopaminergic tone (i.e.: increased DA and DOPAC levels) and improves behavioral performance (i.e.:
77 , a decrease in the concentrations of DA and DOPAC was detected in the inner zone of the AL (AL-IZ).
78 nimals, basal extracellular levels of DA and DOPAC were significantly decreased in two groups of aged
79 icantly reduced striatal TH activity, DA and DOPAC, but there were no significant differences in the
81 n combination, on striatal dopamine (DA) and DOPAC levels, and the density of tyrosine hydroxylase (T
82 levels were not significantly decreased, and DOPAC and HVA levels were decreased by only 65% and 30%,
85 ine (EPI), DHPG, dihydroxyphenylalanine, and DOPAC levels by 4.3, 7.3, 2.5, 0.6 and 1.8-fold and PVN
86 Elevated cysteinyl adducts to L-DOPA and DOPAC are seen early and are followed by increased stria
89 duced striatal reduced striatal dopamine and DOPAC concentrations, regardless of hormonal condition o
90 alone failed to alter striatal dopamine and DOPAC concentrations, with levels obtained being similar
93 dependent reduction of striatal dopamine and DOPAC levels but did not alter HVA, 5-HT, or 5-HIAA.
96 rvival, and striatal and nigral dopamine and DOPAC levels, were evaluated 2 weeks after the lesions.
97 ereotypy, and nucleus accumbens dopamine and DOPAC release responses to an injection of saline follow
98 led to a reduction of striatal dopamine and DOPAC that were both non-significantly greater than that
101 significant increases in the 5-HIAA/5-HT and DOPAC/DA ratios, often used as measures of turnover.
102 tion, DA was not altered but DOPAC level and DOPAC/DA turnover ratios were significantly reduced.
104 the increase in the DOPAC and HVA levels and DOPAC/dopamine ratio induced by L-DOPA in the substantia
105 while the striatal DOPAC and HVA levels and DOPAC/dopamine ratio were significantly reduced as compa
108 er mTBI or injection, DA was not altered but DOPAC level and DOPAC/DA turnover ratios were significan
110 epinephrine (Epi) or monoamine catabolites (DOPAC, 5-HIAA) at any ammonia concentrations tested.
113 al cortex of adult rats, basal levels of DA, DOPAC and HVA did not differ across prenatal treatments;
118 th estrogen had the opposite effect of DHTP, DOPAC/DA and MHPG/NE ratios increased to a greater level
119 its metabolites, 3,4-dihydroxyphenylalanine (DOPAC) and homovanillic acid (HVA); norepinephrine (NE)
121 ridone on ex vivo tissue levels of dopamine, DOPAC, HVA, 5-HT and 5-HIAA in multiple brain regions.
122 (at 6 and 12 h) increase in median eminence DOPAC concentrations in these animals which was blocked
123 administration of PRL-AB on median eminence DOPAC concentrations suggesting that the tonic stimulato
124 olactinemia) failed to alter median eminence DOPAC concentrations unless prolactin exposure was reins
126 ere accompanied by declines in extracellular DOPAC concentrations, and these declines were the same 2
127 haloperidol exposure increased extracellular DOPAC, and this haloperidol-stimulated DOPAC increase wa
129 uenced the effect of D-AMPH on extracellular DOPAC, as the D-AMPH-related decreases in DOPAC were gre
131 e compounds with 1,2-dihydroxyphenyl groups (DOPAC and catechol), their 1,4-dihydroxyphenyl isomers (
132 se in DA turnover, as indicated by a higher (DOPAC+HVA)/DA ratio, seems to be associated to rotenone-
134 ne/metabolite ratios (DOPAC/dopamine and HVA+DOPAC/dopamine) changed with E2 plasma levels, except fo
136 by DNQX was not associated with a change in DOPAC/DA level in the nucleus accumbens or the striatum.
138 e catabolism (as assessed by the decrease in DOPAC and HVA levels) in the striatum and substantia nig
139 was accompanied by a pronounced decrease in DOPAC concentrations in the median eminence of females,
140 PAC in the median eminence and a decrease in DOPAC in the nucleus accumbens; surgical deafferentation
141 ar DOPAC, as the D-AMPH-related decreases in DOPAC were greater for a concentration when it was admin
142 trast to that of dopamine, no differences in DOPAC concentrations between estrogen and non-estrogen-t
143 nelorane caused a dose-dependent increase in DOPAC in the median eminence and a decrease in DOPAC in
146 increases were characterized by increases in DOPAC, HVA, MHPG and 5-HIAA coupled with decreases in DA
149 e CSF measured higher levels of DA and lower DOPAC/DA ratios among the heavy drinkers at the same tim
152 centrations of DA and its primary metabolite DOPAC were determined by high-performance liquid chromat
153 re was an increase in a dopamine metabolite, DOPAC and histologically, DA axons in the striatum were
155 lar levels of dopamine, dopamine metabolites DOPAC and HVA, and the major 5-HT metabolite 5-HIAA, in
156 ochemical analyses of DA and its metabolites DOPAC and HVA show that exercise also functionally prote
157 t depletion of dopamine, and its metabolites DOPAC and HVA, as well as the significant formation of 3
158 ls of striatal dopamine and its metabolites (DOPAC and HVA) following MPTP treatment as determined by
159 ults; however, the levels of DA metabolites, DOPAC, HVA, and the serotonin metabolite, 5-HIAA, were m
160 e depletion of dopamine and its metabolites, DOPAC and HVA and the formation of 3-NT in PC12 cells.
161 The levels of dopamine and its metabolites, DOPAC and HVA were analyzed by HPLC equipped with electr
163 ess, 6-OHDA-induced increases in neostriatal DOPAC/DA and HVA/DA ratios were normalized by age/food-d
167 nt-treated suicides, lower concentrations of DOPAC were observed in the basal ganglia, reaching stati
168 oxidation of DOPAC, and the oxidized form of DOPAC (the quinone) is responsible for the fibrillation
171 mg/kg s.c.) also increased tissue levels of DOPAC, HVA and 5-HIAA by 169, 221 and 134% of basal leve
172 istration of LY379268, mPFC tissue levels of DOPAC, HVA and 5-HIAA were increased in a dose-dependent
174 Syn accelerates the spontaneous oxidation of DOPAC, and the oxidized form of DOPAC (the quinone) is r
178 In addition, there were no changes of DA or DOPAC in the outer zone of the AL (AL-OZ) due to sucklin
179 r basal tissue concentrations of dopamine or DOPAC or the DOPAC:dopamine ratio in either the nucleus
180 effects on mitochondria-catalyzed 5-HIAA or DOPAC formation and hamster ethanol intake reveals a pos
181 ion-the stronger the inhibition on 5-HIAA or DOPAC formation, the greater the ethanol intake suppress
182 ethanol intake and inhibition of 5-HIAA (or DOPAC) formation by six structural analogues of daidzin
183 suggest that HT and its degradation product DOPAC could have a relevant role in preventing the forma
185 Moreover, both dopamine turnover ratios (DOPAC/DA, HVA/DA) and the serotonin turnover ratio (5-HI
187 ed dopamine turnover, as judged from reduced DOPAC levels, in depressed suicides, although we cannot
189 lular DOPAC, and this haloperidol-stimulated DOPAC increase was also greatly attenuated at 6 compared
191 al dopamine was increased while the striatal DOPAC and HVA levels and DOPAC/dopamine ratio were signi
192 rcle determinations, with the exception that DOPAC levels from Orchidectomized mice were significantl
193 ible explanation for this phenomenon is that DOPAC stabilizes the normally transient oligomers and pr
194 of the alpha-Syn Y39W variant suggests that DOPAC binds non-covalently to the same N-terminal region
197 In animals injected with oPRL at 0900 h, the DOPAC/DA ratio increased in the ME, IL and NL within 1 h
198 bitors also counteracted the increase in the DOPAC and HVA levels and DOPAC/dopamine ratio induced by
201 lopride caused a significant increase in the DOPAC/DA ratio in the striatum and nucleus accumbens in
202 mouse retinae a significant increase in the DOPAC/DA ratio is observed following in vivo light stimu
203 OPAC) and homovanillic acid (HVA) and in the DOPAC/dopamine ratio in the putamen, caudate and substan
204 pressure stress significantly increased the DOPAC:dopamine ratio in the nucleus accumbens shell of l
205 e concentrations of dopamine or DOPAC or the DOPAC:dopamine ratio in either the nucleus accumbens cor
207 xidative metabolic conversion of dopamine to DOPAC by the mitochondrial enzyme, monoamine oxidase.