ライフサイエンスコーパス: HVA

1 HVA levels increased with treatment in some affected ind

2 HVA peak current densities in tg and stg were increased

3 levels of DA metabolites homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) reflecte

4 BP) with plasma levels of homovanillic acid (HVA) and clinical symptoms.

5 the dopamine metabolites homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC), in five bra

6 ylacetic acid (DOPAC) and homovanillic acid (HVA) and in the DOPAC/dopamine ratio in the putamen, cau

7 lacetic acid (DOPAC), and homovanillic acid (HVA) by 76%, 53% and 40%, respectively, in the striatum

8 ylacetic acid (DOPAC) and homovanillic acid (HVA) in caudate nucleus resulting from the METH treatmen

9 age percentage of labeled homovanillic acid (HVA) in lumbar cerebrospinal fluid (CSF) was 54% (SD, 9%

10 or to sacrifice increased homovanillic acid (HVA) levels in the left medial prefrontal cortex (mPFC)

11 points and an increase in homovanillic acid (HVA) or 5-hydroxyindoleacetic acid (5-HIAA) concentratio

12 CSF concentration of homovanillic acid (HVA) was significantly lower in the Lewy body variant pa

13 f the dopamine metabolite homovanillic acid (HVA) were decreased in severely affected patients and in

14 f the dopamine metabolite homovanillic acid (HVA) were determined in 30 recently abstinent cocaine-de

15 CSF homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy

16 henylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and serotonin

17 hes were analyzed for DA, homovanillic acid (HVA), and DA activity (HVA/DA) using HPLC.

18 uramine, norfenfluramine, homovanillic acid (HVA), cortisol, and prolactin were determined.

19 f the dopamine metabolite homovanillic acid (HVA), in an extended inbred vervet monkey (Chlorocebus a

20 doleacetic acid (5-HIAA), homovanillic acid (HVA), or 3-methoxy-4-hydroxyphenylgycol (MHPG).

21 ylacetic acid (DOPAC) and homovanillic acid (HVA), were elevated over the same time period.

22 ylacetic acid (DOPAC) and homovanillic acid (HVA), were found to be decreased by >95% in the right pu

23 es, followed by DOPAC and homovanillic acid (HVA).

24 ylacetic acid (DOPAC) and homovanillic acid (HVA).

25 ylacetic acid (DOPAC) and homovanillic acid (HVA).

26 phenylalanine (DOPAC) and homovanillic acid (HVA); norepinephrine (NE) and its metabolite 3-methoxy-4

27 ylacetic acid (DOPAC) and homovanillic acid (HVA)] levels and tyrosine hydroxylase (TH) expression in

28 Plasma homovanillic acid (HVA, a dopamine metabolite), adrenocorticotropic hormone

29 ), and 4-hydroxy-3-methoxyphenylacetic acid (HVA) were significantly diminished in the striata of the

30 acid [5-HIAA]), dopamine (homovanillic acid [HVA]), and norepinephrine (3-methoxy-4-hydroxyphenylglyc

31 High voltage activated (HVA) Ca2+ channels are composed of a pore-forming alpha

32 High voltage activated (HVA) Ca2+ channels are composed of a pore-forming alpha1

33 ip characteristic of high-voltage activated (HVA) Ca2+ channels.

34 patients displayed a high-voltage activated (HVA) Ca2+ conductance with a pronounced Ca2+-dependent i

35 ategorized as either high-voltage activated (HVA) or low-voltage activated (LVA), and a subtype (or s

36 o calcium influx via high-voltage-activated (HVA) (N- and P/Q-type) calcium channels and calcium-acti

37 of two components: a high voltage-activated (HVA) and a low voltage-activated (LVA) calcium current.

38 Both high voltage-activated (HVA) and low voltage-activated (LVA) calcium currents we

39 ns express prominent high-voltage-activated (HVA) and small low-voltage-activated (LVA) macroscopic (

40 nd OFF cells express high-voltage-activated (HVA) Ca(2+) channels, only OFF RGCs also express low-vol

41 ns potently inhibits high voltage-activated (HVA) Ca(2+) channels, providing a powerful means of modu

42 iated exclusively by high-voltage-activated (HVA) Ca(2+) channels.

43 =20 ms) that evoked high-voltage-activated (HVA) Ca(2+) currents (I(Ca)) and elevations in intracell

44 in several genes for high-voltage-activated (HVA) Ca2+ channel subunits are linked to spike-wave seiz

45 High voltage-activated (HVA) Ca2+ current (ICa) was recorded from neonatal rat h

46 nt inhibition of the high voltage-activated (HVA) Ca2+ current, with little or no effect on the low v

47 endent inhibition of high voltage-activated (HVA) Ca2+ currents in Xenopus laevis embryo spinal neuro

48 of inhibition of the high voltage-activated (HVA) Ca2+ currents were produced by 5-HT.

49 density of high threshold voltage-activated (HVA) calcium (Ca(2+)) channels was markedly enhanced in

50 fects of riluzole on high voltage-activated (HVA) calcium channels of rat dorsal root ganglion neuron

51 High-voltage-activated (HVA) calcium channels represent an important class of co

52 -activated (LVA) and high-voltage-activated (HVA) calcium current (I(Ca)).

53 ude of the high-threshold voltage-activated (HVA) calcium current.

54 High-voltage-activated (HVA) calcium currents were recorded from acutely dissoci

55 annel subunits alter high-voltage-activated (HVA) calcium currents, impair neurotransmitter release,

56 -activated (LVA) and high-voltage-activated (HVA) calcium currents.

57 -activated (LVA) and high voltage-activated (HVA) components of calcium current were decreased, demon

58 nd -70 mV as well as high voltage-activated (HVA) current with an activation voltage around -30 mV.

59 n reversibly reduced high-voltage-activated (HVA) currents to 33 +/- 5 % (n = 40) of the control leve

60 T currents), but not high-voltage-activated (HVA) currents.

61 ecific components of high voltage-activated (HVA) IBa, pharmacologically isolated by use of Ca2+ chan

62 predominantly of the high-voltage-activated (HVA) type, which could be carried by Ba2+ and inhibited

63 pressing PP2B, total high-voltage-activated (HVA) VOCCs were suppressed by about 60% at a test potent

64 Ca(2)(+)) influx via high-voltage-activated (HVA), Ca(v)2, channels ("N-, P/Q-, or R-types") that are

65 A, homovanillic acid (HVA), and DA activity (HVA/DA) using HPLC.

66 embrane lipids, via homeoviscous adaptation (HVA), counteracts membrane dysfunction due to temperatur

67 stic precision in Hymenoptera venom allergy (HVA), in particular in patients with double sensitizatio

68 dopamine and DOPAC levels but did not alter HVA, 5-HT, or 5-HIAA.

69 median of 62 points (IQR 39-93; p=0.005) and HVA concentrations by a median of 25 nmol/L (IQR 11-48;

70 Concentrations of CSF 5-HIAA (P = 0.01) and HVA (P < 0.001) were lower in the aggressive group (medi

71 Lower levels of 5-HIAA (P = 0.02) and HVA (P = 0.04) were found in the subgroup of aggressive

72 antly increased anxiety, ACTH, cortisol, and HVA.

73 nduced increases in neostriatal DOPAC/DA and HVA/DA ratios were normalized by age/food-deprivation wh

74 n of dopamine and its metabolites, DOPAC and HVA and the formation of 3-NT in PC12 cells.

75 DOPAC and HVA changes were measured at 1 day and were reversed wit

76 of adult rats, basal levels of DA, DOPAC and HVA did not differ across prenatal treatments; however,

77 o counteracted the increase in the DOPAC and HVA levels and DOPAC/dopamine ratio induced by L-DOPA in

78 e was increased while the striatal DOPAC and HVA levels and DOPAC/dopamine ratio were significantly r

79 e not significantly decreased, and DOPAC and HVA levels were decreased by only 65% and 30%, respectiv

80 sm (as assessed by the decrease in DOPAC and HVA levels) in the striatum and substantia nigra was sim

81 analyses of DA and its metabolites DOPAC and HVA show that exercise also functionally protects neuron

82 s of dopamine and its metabolites, DOPAC and HVA were analyzed by HPLC equipped with electrochemical

83 atal dopamine and its metabolites (DOPAC and HVA) following MPTP treatment as determined by HPLC meth

84 of dopamine, dopamine metabolites DOPAC and HVA, and the major 5-HT metabolite 5-HIAA, in rat medial

85 n of dopamine, and its metabolites DOPAC and HVA, as well as the significant formation of 3-nitrotyro

86 hyperthermia and depletion of DA, DOPAC and HVA.

87 3,4-dihydroxyphenylacetic acid (DOPAC), and HVA levels in rats that exhibited low levels of locomoto

88 ed a significant depletion of DA, DOPAC, and HVA at all time points.

89 One striatum was examined for DA, DOPAC, and HVA levels using HPLC-EC and the contralateral striatum,

90 e no significant differences in dopamine and HVA concentrations in either suicide group compared to c

91 nide, DOPAC-glucuronide, HVA-glucuronide and HVA-sulphate were also detected.

92 ly rejected infants had lower CSF 5-HIAA and HVA than low-rejection infants.

93 concentrations and ratios of HVA/5-HIAA and HVA/MHPG did not significantly change with 6 weeks of ei

94 ur patients reduced both the maximal LVA and HVA Ca2+ conductances in murine dorsal root ganglion neu

95 mined biophysical properties of both LVA and HVA Ca2+ currents in thalamic cells of tottering (tg; Ca

96 d the biophysical properties of both LVA and HVA currents in Cm/+ and wild-type thalamic neurons and

97 DmalphaG is required for regulating LVA and HVA derived from Dmca1A in vivo.

98 Post-mortem CSF 5-HIAA, MHPG and HVA were measured by high-performance liquid chromatogra

99 er IBO, DOPAC concentrations in striatum and HVA levels in the frontal cortex were below control valu

100 anic sites within the Hellenic Volcanic Arc (HVA).

101 r controlling for breed and age of dogs, but HVA differences may have been breed-dependent.

102 increase suppressed by mibefradil but not by HVA Ca2+ channel antagonists.

103 nism is not dependent on, or accompanied by, HVA channel Ca(2)(+) influx, and is insensitive to agoni

104 ealed during acid exposure as the whole-cell HVA current was depressed.

105 hronic stimulation was related to concurrent HVA plasma elevations, implying DBS-induced dopamine rel

106 CSF HVA is an index of CNS dopamine activity, which is hypot

107 by the genome scan, we mapped a QTL for CSF HVA at a genome-wide level of significance (peak logarit

108 In a similar manner, labeled CSF HVA concentrations were not influenced by duration of di

109 Labeled CSF HVA levels did not significantly correlate with either q

110 +/- 15 pmol/mL; P< or =.001) but normal CSF HVA and MHPG concentrations.

111 gnificantly higher mean concentration of CSF HVA than did the healthy comparison group.

112 idal side effects and have low levels of CSF HVA.

113 Their CSF HVA concentrations averaged only 54% of the concentratio

114 er, both dopamine turnover ratios (DOPAC/DA, HVA/DA) and the serotonin turnover ratio (5-HIAA/5-HT) w

115 A-mediated currents varied with time of day; HVA currents in cells from OVX+E mice were lower than th

116 e acidosis (pH 6.9-6.0) reversibly depressed HVA Ca2+ current amplitude and caused a positive shift i

117 ctivity exhibited by (+)-ACN among different HVA current components suggests that manipulations of st

118 reperfusion increase in DA turnover (DOPAC + HVA/DA) at 5 min after reperfusion.

119 DA turnover, as indicated by a higher (DOPAC+HVA)/DA ratio, seems to be associated to rotenone-induce

120 In the adult, basal levels of DA, DOPAC, HVA and 5-HIAA in n. accumbens did not differ across pre

121 on ex vivo tissue levels of dopamine, DOPAC, HVA, 5-HT and 5-HIAA in multiple brain regions.

122 es were characterized by increases in DOPAC, HVA, MHPG and 5-HIAA coupled with decreases in DA, NE an

123 owever, the levels of DA metabolites, DOPAC, HVA, and the serotonin metabolite, 5-HIAA, were markedly

124 s.c.) also increased tissue levels of DOPAC, HVA and 5-HIAA by 169, 221 and 134% of basal levels in n

125 on of LY379268, mPFC tissue levels of DOPAC, HVA and 5-HIAA were increased in a dose-dependent manner

126 the amygdala and hippocampus, and dopamine (HVA/DA, DOPAC/DA) in prefrontal cortex.

127 esignation of L-type channels as exclusively HVA and reveal a possible role in subthreshold Ca2+ sign

128 ga-Conotoxin-MVIIC, a nonselective toxin for HVA channels, had no effect on either of the LVA current

129 to controls, although there was a trend for HVA concentrations to be lower in suicides.

130 In both genotypes, HVA currents were predominantly of the omega-agatoxin-IV

131 HT-glucuronide, DOPAC-glucuronide, HVA-glucuronide and HVA-sulphate were also detected.

132 ession, function and responsiveness of high (HVA)- and low-voltage-activated (LVA) Ca2+ channels to I

133 via high-voltage-activated Ca2+ channels (I(HVA)).

134 high-voltage-activated barium currents (IBa, HVA) in tiger salamander retinal ganglion cells.

135 very from inactivation of LVA currents or in HVA current densities and kinetics.

136 OVX+E mice with estradiol rapidly increased HVA currents primarily through L- and R-type VGCCs by ac

137 release, which was associated with increased HVA plasma levels and improved clinical symptoms, sugges

138 te altered the ability of (+)-ACN to inhibit HVA current in dorsal root ganglion neurons, indicating

139 ates K+ channels and simultaneously inhibits HVA Ca2+ channels via different receptor subtypes.

140 The mean CSF labeled HVA concentration was 34.7 ng/ml (SD, 20.2 ng/ml; range,

141 beled serum LD closely predicted CSF labeled HVA concentrations (r = 0.747, p = 0.033).

142 Third, mRNA levels of lamprey HVA calcium and SKKCa channels in axotomized RS neurons

143 We suggest that a low HVA level is a biological marker with modest association

144 In contrast, in OVX+E mice, HVA-mediated currents varied with time of day; HVA curre

145 iting without warning (5-HIAA 196.0 pmol/ml; HVA 302.0 pmol/ml) compared to dogs that warned (5-HIAA

146 group (median values: 5-HIAA 202.0 pmol/ml; HVA 318.0 pmol/ml) than in controls (5-HIAA 298.0 pmol/m

147 d to dogs that warned (5-HIAA 244.0 pmol/ml; HVA 400.0 pmol/ml).

148 /ml) than in controls (5-HIAA 298.0 pmol/ml; HVA 552.0 pmol/ml).

149 herefore operate in parallel with the normal HVA-dependent processes.

150 that N(2)O selectively blocks T-type but not HVA Ca(2+) currents in small sensory neurons and Ca(v)3.

151 ere were no diurnal changes in any aspect of HVA-mediated I(Ca) in OVX mice.

152 and beta 2a induce a sustained component of HVA current, and alpha 2-delta also influences the volta

153 a and beta2a induce a sustained component of HVA current, and alpha2-delta also influences the voltag

154 Smokers' low CSF concentrations of HVA may be associated either with chronic inhalation of

155 no significant changes in concentrations of HVA.

156 The depression of HVA Ca2+ currents by low pHo was unaffected by raising t

157 ) subunit captures the functional essence of HVA calcium channels, and introduce alpha(1)-Ca(V)beta f

158 ctivity does not influence the expression of HVA Ca2+ channels, but modulates their function by Ca(2+

159 The finding of HVA calcium channels distributed throughout the whole de

160 ed cells induced an up to 5-fold increase of HVA VOCCs.

161 ated during the second scan, while levels of HVA and cortisol were not altered significantly during t

162 y examines whether subunit protein levels of HVA Ca(2+) channels are altered in IC neurons that exhib

163 we examined the subcellular localization of HVA calcium channels by using immunocytochemistry at the

164 these results suggest that the modulation of HVA by the JMD could be mediated by changes in the statu

165 , CSF monoamine concentrations and ratios of HVA/5-HIAA and HVA/MHPG did not significantly change wit

166 ribute to the overall feedback regulation of HVA-mediated I(Ca) by estradiol.

167 ivated (LVA), and a subtype (or subtypes) of HVA Ca2+ channels link the presynaptic depolarization to

168 enhanced current density of L- and R-type of HVA Ca(2+) channels in IC neurons of the GEPR, and may c

169 The effects of 5-HT on HVA Ca2+ currents were mediated by 5-HT1A and 5-HT1D rec

170 Inactivation time constants and peak HVA Ca2+ current (ICa) amplitudes did not differ between

171 kers had markedly lower CSF, but not plasma, HVA levels.

172 The conductance ratio of the presynaptic HVA current was 0.9, significantly lower that that of th

173 s of DA and DOPAC, while it slightly reduced HVA concentration.

174 onsiderably more negative than the remaining HVA current.

175 At this membrane voltage, a second HVA current was revealed during acid exposure as the who

176 Half-blockade of (+)-ACN-sensitive HVA current occurred in the range of 3-25 microM, with N

177 Ba2+/Ca2+ conductance ratios of the somatic HVA and LVA channels were 1.4 and 0.7, respectively.

178 significantly lower that that of the somatic HVA current.

179 annels accounted for only 6 % of the somatic HVA, while L-, N- and R-type Ca2+ channels each accounte

180 nce of SWDs and that altered somatodendritic HVA currents are not required for abnormal thalamocortic

181 eceptor selective agonist, DAMGO, suppressed HVA IBa (in 64/71 neurones) in a naloxone-reversible and

182 , while lowering extracellular pH suppressed HVA Ca2+ currents, Zn2+ current amplitude was affected o

183 Telencephalic HVA as well as the HVA/DA ratio were also significantly

184 The HVA current remaining in LES-treated motoneurons was lit

185 The HVA current was inactivated completely at a holding pote

186 The HVA is geologically and ecologically unique, with report

187 Telencephalic HVA as well as the HVA/DA ratio were also significantly greater in dominant

188 1A, alpha 1B and alpha 1E genes encoding the HVA Ca2+ channels P/Q, N and R, respectively, but not al

189 nature and origin of these compounds in the HVA.

190 Riluzole at 30 microM inhibited the HVA currents.

191 rsibly reduced 34 +/- 1.6 % (n = 102) of the HVA Ca2+ currents.

192 All of the HVA current subtypes are expressed in bushy cells, but t

193 The activation threshold of the HVA current was at -40 mV.

194 Riluzole inhibition of the HVA currents was abolished and partially reduced by addi

195 Riluzole inhibition of the HVA currents was also blocked by internal application of

196 nd shifting of the voltage dependence of the HVA currents.

197 ay be involved in riluzole inhibition of the HVA currents.

198 t affect riluzole's inhibitory effect on the HVA currents.

199 addition, we show that Dmca1A underlies the HVA somatodendritic calcium currents in vivo.

200 ctive organic antagonists of high-threshold (HVA) Ca2+ channels, nimodipine, omega-Conotoxin GVIA, an

201 Thus HVA VOCCs, in a phosphorylated state under control condi

202 somewhat less effective at inhibiting total HVA current than (+)-ACN, whereas several steroid analog

203 e relatively ineffective at inhibiting total HVA current.

204 with antibodies against P/Q-, N-, and R-type HVA calcium channels demonstrated the presence of these

205 Drosophila Ca(v)2 homolog, Dmca1A, underlies HVA and LVA somatodendritic calcium currents in the same

206 2+ current as well as a further unidentified HVA current that was insensitive to dihydropyridines, om

207 lective, more potent, small-molecular-weight HVA channel blockers.

208 composition patterns are not consistent with HVA expectations and suggest a stress response.

209 ociated protein (SNAP25) that interacts with HVA channels, reveals abnormal spike-wave discharges (SW