ライフサイエンスコーパス: L-dopa

1 r and standard anti-Parkinson drug levodopa (l-DOPA).

2 ated uptake of a model substrate into cells (L-DOPA).

3 rosine to form l-3,4-dihydroxyphenylalanine (l-DOPA).

4 function and sometimes remedied by levodopa (L-DOPA).

5 e (DHPAA) from L-3,4-dihydroxyphenylalanine (L-DOPA).

6 hitin via any chemical process (tyrosine and l-DOPA).

7 catalyzes the hydroxylation of L-tyrosine to L-DOPA.

8 obtained with the optimal dose of peripheral l-DOPA.

9 ents known as dyskinesia upon treatment with L-DOPA.

10 esence of dyskinesias even in the absence of L-dopa.

11 ursors and metabolites as norepinephrine and l-DOPA.

12 or impairment that was partially reversed by l-DOPA.

13 ed in pancreatic beta-cells from circulating L-dopa.

14 denervation and pulsatile administration of L-DOPA.

15 while maintaining the therapeutic effect of L-DOPA.

16 akly dyskinetic animals after treatment with L-DOPA.

17 s without altering normal motor responses to L-DOPA.

18 fering with the therapeutic motor effects of L-DOPA.

19 ing a negative feedback on ERK activation by l-DOPA.

20 out compromising the therapeutic efficacy of L-DOPA.

21 result from diverse mechanisms of action of L-dopa.

22 iatal Nurr1 despite receiving a high dose of l-DOPA.

23 se patients (N = 15) who received 3 weeks of L-DOPA.

24 nrichment of an enzyme-coupled biosensor for L-DOPA.

25 neuronal cells and the PD-relevant stressor, L-DOPA.

26 d a progressive motor disorder responsive to l-DOPA.

27 [(18)F]6-fluoro-L-DOPA ([(18)F]FDOPA) is a diagnostic radiopharmaceutica

28 pamine synthesis and storage ((18)F-6-fluoro-L-dopa; (18)F-FDOPA).

29 conditions: 150 mg of the dopamine precursor L-dopa, 2 mg of the D2 receptor antagonist haloperidol,

30 h 6-hydroxydopamine lesions during long-term L-DOPA (25 mg/kg) treatment.

31 ptor antagonist, with the dopamine precursor l-DOPA (25, 100, and 200 mg) or applied placebo medicati

32 We previously proposed that l-DOPA 4,5-dioxygenase activity evolved via a single Car

33 repeated convergent acquisition of elevated l-DOPA 4,5-dioxygenase activity is consistent with recur

34 We find that low l-DOPA 4,5-dioxygenase activity is distributed across th

35 rise to polyphyletic occurrences of elevated l-DOPA 4,5-dioxygenase activity, accompanied by converge

36 The evolution of l-DOPA 4,5-dioxygenase activity, encoded by the gene DOD

37 characterised 23 distinct DODA proteins for l-DOPA 4,5-dioxygenase activity, from four betalain-pigm

38 phylogeny, we then explored the evolution of l-DOPA 4,5-dioxygenase activity.

39 processing and gait speed were observed with L-DOPA (450-mg dose: processing speed factor score effec

40 The use of l-DOPA, a small molecule drug shown to up-regulate VEGF

41 NAc slices reveal that both in vivo systemic l-DOPA administration and in vitro exposure to dopamine

42 erneurons become dysregulated during chronic L-DOPA administration and participate in the expression

43 In parkinsonian rats, l-DOPA administration reduced M1 glutamate efflux and en

44 ch were assessed for LID following long-term L-DOPA administration.

45 functioning by l-3,4-dihydroxyphenylalanin (l-DOPA) administration during early withdrawal.

46 g-term treatment of Parkinson's disease with l-DOPA almost always leads to the development of involun

47 Subjects receiving L-dopa also progressed slower through the training and t

48 l-DOPA also reverses the selective loss of dendritic "lo

49 gic neuromodulation by systemic injection of L-DOPA and Carbidopa (LDC) or by local application of DA

50 on's disease, serotonergic terminals take up L-DOPA and convert it to dopamine.

51 lectrode fouling caused by polymerization of L-DOPA and endogenous catecholamines on the electrode su

52 orsened locomotor performance in response to L-DOPA and enhanced LID scores.

53 st Parkinson's disease patients will receive l-DOPA and eventually develop hyperkinetic involuntary m

54 e confirmed increased Nptx2 expression after L-DOPA and its blockade by SL327 using quantitative RT-P

55 luate changes in dopamine release induced by l-DOPA and l-DOPA+dextroamphetamine.

56 e it is a genetic modifier of sensitivity to l-DOPA and of nicotine neuroprotection in PD.

57 ns and attenuates the behavioral response to l-DOPA and presynaptic and postsynaptic glutamate neurot

58 ional program in striatal neurons induced by L-DOPA and triggered by the activation of ERK.

59 rovement in the dystonia in response to both l-DOPA and trihexyphenidyl.

60 s of dopamine by administering its precursor l-DOPA and/or dopamine D2-receptor agonists.

61 minergic neurons, the behavioral response to l-DOPA, and presynaptic and postsynaptic glutamate neuro

62 eran insects demonstrated that low levels of l-DOPA are rapidly metabolized into intermediates by phe

63 Using l-DOPA as a model substrate, biochemical assays in large

64 By boosting dopamine levels using levodopa (l-DOPA) as human subjects made economic decisions and re

65 Administration of the dopamine precursor L-DOPA at a dose that replenished dopamine signaling in

66 Mixtures of DA and L-DOPA at different molar rations were co-electropolymer

67 Instead, L-dopa attenuated neural representations of overall unce

68 eliable tool that allows a better measure of L-DOPA augmented dopamine release in vivo, measured usin

69 ndomly allocated to either receive 100/25 mg L-dopa/benserazide (n = 32) or placebo (n = 31) prior to

70 arkinson's patient microbiotas and increases l-dopa bioavailability in mice.

71 We found that prefrontal tDCS and l-DOPA both enhance neural activity in core regions of t

72 -THP in a single enzyme system directly from L-DOPA both in vitro and in vivo, at higher yields than

73 (DA) precursor l-3,4-dihydroxyphenylalanine (L-DOPA), but its prolonged use causes dyskinesias referr

74 hibit tremor and rotational responses toward L-DOPA, but develop less dyskinesia.

75 Reference intervals for l-DOPA, catecholamines, and metanephrines in n = 115 hea

76 simultaneous quantification of unconjugated l-DOPA, catecholamines, and metanephrines in plasma by L

77 We find that L-DOPA causes parkin loss through both oxidative stress-

78 he NM-MRI signal 3 weeks post-treatment with L-DOPA compared to baseline (200 of 1807 SN-VTA voxels;

79 TcKO mice was alleviated by donepezil and by l-DOPA, confirming an acetylcholine/dopamine deficit.

80 Moreover, coadministration of rapamycin with L-DOPA counteracts L-DOPA-induced dyskinesias in wild-ty

81 fied glassy carbon electrodes to form a poly(L-DOPA/DA) film.

82 decarboxylase does not prevent gut microbial l-dopa decarboxylation, we identified a compound that in

83 cy of adeno-associated viral vector-mediated l-DOPA delivery to the putamen in 1-methyl-4-phenyl-1,2,

84 The synthesis of a protected analog of l-DOPA demonstrates the utility of AHF for enantioselect

85 l-DOPA-dependent deregulation of 28 genes was blocked by

86 ent evidence links LID to excessive striatal L-dopa-derived dopamine (DA) release, while the possibil

87 es in dopamine release induced by l-DOPA and l-DOPA+dextroamphetamine.

88 Among sham-lesioned rats, l-DOPA did not change glutamate or GABA efflux.

89 stimating equations tested the pre- and post-L-DOPA differences in processing and gait speed measures

90 Microinjection of l-DOPA directly into the striatum ameliorated the dyston

91 Using an escalating L-DOPA dose protocol, LID severity was decreased in Narp

92 Supplying l-DOPA during withdrawal re-establishes synaptic morphol

93 ring frequency significantly increased in ON L-DOPA dyskinetic 6-hydroxydopamine-lesioned rats, sugge

94 Because L-DOPA effects may be influenced by body weight, we repe

95 We previously reported that L-DOPA effects on reward-based decision-making in a rand

96 ted that baseline impulsivity would moderate L-DOPA effects.

97 The impact of DREAM on L-DOPA efficacy was evaluated using the rotarod and the

98 r catecholamine neurotransmitters, including L-DOPA, epinephrine, and norepinephrine.

99 esia (LID) develops after repeated levodopa (l-DOPA) exposure in Parkinson disease patients and remai

100 ation that develops after repeated levodopa (l-DOPA) exposure in Parkinson disease patients.

101 We obtained baseline 6-[(18)F]fluoro-L-DOPA (FDOPA)-PET scans in 15 nonsmokers and 30 nicotin

102 ositron emission tomography followed by open L-DOPA for 3 weeks (1 week each of 150 mg, 300 mg, and 4

103 While CYP76AD1 catalyzes both l-DOPA formation and its subsequent conversion to cyclo-

104 l-DOPA formation in red beet was found to be redundantly

105 concentration in the cerebrospinal fluid of L-DOPA-free PD patients.

106 rains produced 0.91 g/L tyrosine or 0.41 g/L l-DOPA from 22.5 g/L unpurified SSW-derived chitin hydro

107 and treatment whereby, among lesioned rats, l-DOPA given acutely (1 d) or chronically (14-16 d) redu

108 Following L-DOPA, global p11KO mice show reduced therapeutic respo

109 movements but cerebellar microinjections of l-DOPA had no effect.

110 In support of our hypothesis, L-DOPA had no main effect on impulsive choice, but reduc

111 An acute dose of 5 mg/kg L-DOPA had no significant effect on dopamine dynamics, d

112 L-DOPA has been the gold standard for symptomatic treatm

113 course analysis (0-6 h after treatment with L-DOPA) identified an acute signature of 709 genes, amon

114 red to the placebo group, subjects receiving L-dopa improved less in spatial intelligence (-0.267 SDs

115 By enhancing availability of dopamine, L-DOPA improved processing and gait speed in older adult

116 supplementation with the dopamine-precursor L-dopa improves effects of cognitive training on perform

117 oral delivery, can be avoided by delivering l-DOPA in a more continuous manner.

118 e, we assessed the roles of the DA precursor L-DOPA in beta-cell DA synthesis and release in conjunct

119 of iSPNs abolished the therapeutic action of L-DOPA in PD mice.

120 We also assessed how ocSSRT responded to L-dopa in PD patients and botulinum toxin injections in

121 The enhanced behavioral sensitization to l-DOPA in TAAR1 KO mice was paralleled by increased phos

122 riatal neurons and in vivo on the effects of L-dopa in the 6OHDA (6-hydroxydopamine) contralateral tu

123 s not depend directly on the availability of l-Dopa in the basal ganglia.

124 identified a molecular signature induced by L-DOPA in the dopamine-denervated striatum that is depen

125 lator of cholinergic activity in response to L-DOPA in the dopamine-depleted parkinsonian brain.

126 This novel finding suggests the utility of l-DOPA in the field of implantable medical devices, such

127 lay major roles in the cellular responses to l-DOPA in the striatum, these findings prompted us to ex

128 Subchronic L-DOPA increases levels of adaptor protein p11 (S100A10)

129 Our findings suggest that D5R can modulate L-DOPA induced dyskinesia and is a critical activator of

130 d how it affects cholinergic interneurons in L-DOPA induced dyskinesia, we used D5R knockout mice tha

131 tration and participate in the expression of L-DOPA induced dyskinesia.

132 ly involved in L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson's disease

133 mouse model of L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson's disease

134 3,4-Dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia (LID) is a debilitating side

135 disease and in l-3,4-dihydroxyphenylalanine (l-DOPA)-induced dyskinesia (LID), a common motor complic

136 implicated in 3,4-dihydroxy-l-phenylalanine (L-DOPA)-induced dyskinesia (LID), a motor complication a

137 ly involved in L-3,4-dihydroxyphenylalanine (L-Dopa)-induced dyskinesia (LID), the debilitating side-

138 L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia is an incapacitating complica

139 evelopment of 3,4-dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia.

140 in the dorsal striatum dramatically reduced l-dopa-induced abnormal involuntary movements compared w

141 stical parametric maps, indicating tDCS- and l-DOPA-induced activation, and >100 neuronal receptor ge

142 ulation in rodent models of PD (PD mice) and L-DOPA-induced dyskinesia (LID mice).

143 ficacy decreases, and side effects including l-DOPA-induced dyskinesia (LID) increase, affecting up t

144 triatonigral neurons reduces the severity of l-DOPA-induced dyskinesia (LID), a finding that correlat

145 therapy is complicated by the appearance of L-DOPA-induced dyskinesia (LID).

146 nduced in the striatum of rodents expressing l-DOPA-induced dyskinesia (LID).

147 dered Parkinsonian nonhuman primate model of l-DOPA-induced dyskinesia (PD-LID).

148 The protein DREAM decreases development of L-DOPA-induced dyskinesia in mice and reduces L-DOPA-ind

149 s such as Huntington's disease, dystonia and l-DOPA-induced dyskinesia in Parkinson's disease are all

150 ovide therapeutic approaches for alleviating L-DOPA-induced dyskinesia in PD patients.

151 Overall, the present study demonstrates that l-DOPA-induced dyskinesia is associated with increased M

152 In daDREAM mice, L-DOPA-induced dyskinesia was decreased throughout the e

153 ic microinjections into M1 demonstrated that l-DOPA-induced dyskinesia was reduced by M1 infusion of

154 at activate DREAM may be useful to alleviate L-DOPA-induced dyskinesia without interfering with the t

155 development of involuntary movements termed l-DOPA-induced dyskinesia.

156 symptoms of Parkinson's Disease (PD), and to L-DOPA-induced dyskinesia.

157 benefits of RA supplementation in moderating L-DOPA-induced dyskinesia.

158 longed use causes dyskinesias referred to as L-DOPA-induced dyskinesias (LIDs).

159 HT1A and 5-HT1B receptors effectively blocks L-DOPA-induced dyskinesias in animal models of dopamine

160 razine, a 5-HT1A/B receptor agonist, against L-DOPA-induced dyskinesias in patients with Parkinson's

161 tration of rapamycin with L-DOPA counteracts L-DOPA-induced dyskinesias in wild-type mice, but not in

162 ltoprazine caused a significant reduction of L-DOPA-induced dyskinesias on area under the curves of C

163 get to improve motor function while reducing l-dopa-induced dyskinesias.

164 taining neurons underlies the development of L-DOPA-induced dyskinesias.

165 pamine may participate in the development of L-DOPA-induced dyskinesias.

166 ale/six female; 66.6 +/- 8.8 years old) with L-DOPA-induced dyskinesias.

167 tal MOR1 levels and signaling and alleviates L-DOPA-induced dyskinetic movements in pituitary homeobo

168 -DOPA-induced dyskinesia in mice and reduces L-DOPA-induced expression of FosB, phosphoacetylated his

169 represent a promising approach to decreasing L-DOPA-induced motor complications in Parkinson's diseas

170 Conversely, RO5166017 counteracted both l-DOPA-induced rotation and dyskinesia as well as AMPA r

171 e tested daily with L-DOPA to assess LID and L-DOPA-induced rotations.

172 udies with chronic oral eltoprazine to treat l-DOPA-induced-dyskinesias.

173 Chronic L-DOPA induces abnormal spine re-growth exclusively in D

174 Together, these findings demonstrate that l-DOPA induces widespread changes to striatal DNA methyl

175 and even be hyperactive 72 h after the last L-DOPA injection when dopamine was almost completely dep

176 eficient (DD) mice, which had received daily L-DOPA injections, could move effectively and even be hy

177 to a more refined dopaminergic therapy where l-DOPA is delivered continuously at the site where it is

178 Our results show that the uptake of L-DOPA is essential for establishing intracellular DA st

179 creased LHb neuronal activity in response to L-DOPA is related to AIM manifestation.

180 atal neurons.SIGNIFICANCE STATEMENT To date, l-DOPA is the most effective treatment for PD.

181 ent with Levodopa [L-dihydroxyphenylalanine (L-DOPA)] is the gold standard treatment of Parkinson's d

182 e the possibility of a direct involvement of L-dopa itself in LID has been largely ignored.

183 ergic signaling using the dopamine precursor l-DOPA (l-3,4-dihydroxyphenylalanine) or dopamine recept

184 unilateral lesions were then challenged with l-dopa (levodopa) and various dopamine receptor agonists

185 be an interspecies pathway for gut bacterial l-dopa metabolism.

186 s study examined whether carbidopa/levodopa (L-DOPA) monotherapy increased dopamine availability, inc

187 reover, we found that expression of Nurr1 in l-DOPA naive hemi-parkinsonian rats resulted in the form

188 We additionally determined that in l-DOPA-naive rats striatal rAAV-Nurr1 overexpression (1)

189 The constant, local supply of l-DOPA obtained with this approach holds promise as an e

190 rate of ChIs, whereas chronic treatment with L-DOPA of lesioned mice increases baseline ChI firing ra

191 also exhibited baseline-dependent effects of L-DOPA on loss aversion and delay discounting.

192 ole by examining the effect of its precursor L-DOPA on the choices of healthy human participants in a

193 ontaining neurons have a reduced response to L-DOPA on the therapeutic parameters, but develop dyskin

194 amine (DA) and L-3,4-dihydroxyphenylalanine (L-DOPA) on carbon nano-onion (CNO) modified electrodes a

195 gle dose of the dopamine precursor levodopa (l-DOPA) on mesostriatal fractional amplitude of low-freq

196 Application of l-DOPA, on the other hand, increased blood vessel format

197 In the absence of L-DOPA, only chemogenetic stimulation of dSPNs mediated

198 ing) suppresses motor dysfunction induced by L-DOPA or D(2)R-selective agonists.

199 eading to dyskinesia in animals treated with L-DOPA or D1 receptor agonists.

200 Nurr1 agonist amodiaquine (AQ) together with l-DOPA or ropinirole.

201 would occur on haloperidol than on levodopa (l-DOPA) or placebo.

202 were abolished by the antiparkinsonian drug, L-DOPA, or by SKF81297, a dopamine D1-type receptor agon

203 the Parkinson's disease medication Levodopa (l-dopa), potentially reducing drug availability and caus

204 Furthermore, L-DOPA preferentially inhibits DA uptake in lesioned str

205 l-DOPA present in morinda additionally increases the siz

206 isition or expression had taken place, using L-Dopa, primarily, as catecholaminergic precursor.

207 describe a three-round screen for increased L-DOPA production in S. cerevisiae using FACS enrichment

208 eases total heme concentration and increases L-DOPA production, using dopamine measurement as a proxy

209 equently, improved our ability to screen for L-DOPA production.

210 dministration of caffeine with a low dose of l-DOPA reduces dyskinesia in animals with striatopallida

211 opamine function (dihydroxy-L-phenylalanine; L-DOPA) reduces the impact of valence on information-see

212 from the gut microbiota metabolize Levodopa (L-dopa), reducing bioavailability of the drug for treati

213 L-DOPA reinstatement of dopamine normalized HCN activity

214 Restoration of dopamine transmission by l-DOPA relieves symptoms of PD but causes dyskinesia.

215 Restoration of dopamine transmission by l-DOPA relieves symptoms of PD but causes severe side ef

216 ration of dopamine transmission by levodopa (L-DOPA) relieves motor symptoms of PD but often causes d

217 ate and D-serine in the monkey putamen while L-DOPA rescues both D-amino acids levels.

218 ut its role in experimental Parkinsonism and l-DOPA responses has been neglected.

219 inergic transmission, but its role in PD and l-DOPA responses has been neglected.

220 mice, we demonstrate that a progressive and L-dopa-responsive DA deficiency reduces ACh availability

221 ects, we generated a knock-in mouse model of l-DOPA-responsive dystonia (DRD) mice that recapitulates

222 sis of dopamine, including GCH1 and TH cause l-DOPA-responsive dystonia.

223 ause dopaminergic neuron loss and severe but L-DOPA-responsive motor defects in mouse overexpression

224 9S and R1441C mutant transgenic rats exhibit L-DOPA-responsive motor dysfunction, impaired striatal d

225 ns in cultured neurons and causes a PD-like, l-DOPA-responsive motor phenotype in transgenic mice, wa

226 affected offspring suffered from early-onset l-DOPA-responsive Parkinson's disease.

227 transmission could contribute to the reduced L-DOPA responsivity.

228 ernal dopamine metabolism with the precursor l-DOPA, resuming oogenesis and stimulating egg productio

229 ped side effects from their long-term use of L-dopa revealed, in some cases, the presence of dyskines

230 er, administration of the dopamine precursor l-DOPA reversed the presynaptic deficit by restoring the

231 urons in Mutator mice degenerated causing an L-DOPA reversible motor deficit.

232 has enabled rapid and reliable detection of L-DOPA's effects on striatal dopamine signaling in intac

233 tantia nigra pars compacta and age-dependent L-DOPA-sensitive motor dysfunction.

234 Feeding with excess l-DOPA showed that the metabolic intermediate 5,6-dihydr

235 Administration of L-dopa significantly improved ocSSRT and RT in PD patien

236 In contrast, administration of 200 mg/kg L-DOPA significantly increased the amplitude of evoked d

237 in combination with a suprathreshold dose of L-DOPA (Sinemet(R)) in 22 patients with Parkinson's dise

238 o their sustantia nigra or by treatment with l-DOPA, suggesting that alpha-SYN regulates dopamine ava

239 support for learning-enhancing properties of L-dopa supplements in the healthy elderly.

240 -of-principle for continuous vector-mediated l-DOPA synthesis as a novel therapeutic strategy for Par

241 Local gene delivery of the l-DOPA synthesizing enzymes, tyrosine hydroxylase and gu

242 With the discovery of l-dopa the advent of medical therapy began and surgical

243 f phenylalanine into tyrosine, tyrosine into L-dopa (the precursor of dopamine), and tryptophan into

244 Very little is known about how L-DOPA therapy affects the dynamics of fluctuating dopam

245 studying the molecular mechanisms underlying L-DOPA therapy and also promises to benefit a wide varie

246 ia circuits and represents a major target of L-DOPA therapy in Parkinson's disease.

247 Therefore, targeting beta-arrestins in PD L-DOPA therapy might prove to be a desirable approach.

248 Moreover, L-DOPA therapy restored tNAA (9.1 +/- 0.4 vs 8.1 +/- 0.2

249 kinesia is an incapacitating complication of L-DOPA therapy that affects most patients with Parkinson

250 arkers for Parkinson disease and efficacy of L-DOPA therapy.

251 tNAA and tCr levels are responsive to L-DOPA therapy.

252 etic profile or antiparkinsonian efficacy of L-DOPA therapy.

253 ion occurring under dopamine denervation and L-DOPA therapy.

254 n 40 years ago l-3,4-dihydroxyphenylalanine (l-DOPA) therapy has retained its role as the leading sta

255 ion about potential gains than losses, under L-DOPA this difference was not observed.

256 on impulsive choice, we administered 150 mg L-DOPA to 87 healthy adults in a randomized, placebo-con

257 ministration, animals were tested daily with L-DOPA to assess LID and L-DOPA-induced rotations.

258 inistration, the rats were tested daily with L-Dopa to assess LID.

259 Conversion of l-dopa to dopamine by a pyridoxal phosphate-dependent ty

260 ydroxydopamine and subsequently treated with L-DOPA to induce dyskinesia.

261 omography with the radiotracer [(18)F]fluoro-l-DOPA to quantify striatal presynaptic dopamine synthes

262 e of Nurr1 expression in striatal neurons of l-DOPA-treated PD patients.

263 r1 expression can be found in the putamen of l-DOPA-treated PD patients.

264 eurons by ablating them before initiation of L-DOPA treatment and determining whether it decreases LI

265 LTP, depotentiation, and LTP restored after L-DOPA treatment but also disclose multifaceted synaptic

266 nted dopaminergic signaling is revived after l-DOPA treatment during early withdrawal.

267 With time, however, the shortcomings of oral l-DOPA treatment have become apparent, particularly the

268 Our data demonstrate the efficacy of l-dopa treatment in improving sleep disorders in parkins

269 the impact of CK2 ablation on the effects of l-DOPA treatment in the unilateral 6-OHDA lesioned mouse

270 Subchronic l-DOPA treatment of TAAR1 KO mice unilaterally lesioned

271 hemical studies investigating the effects of L-DOPA treatment on electrically evoked dopamine release

272 ent to preliminarily evaluate the effects of L-DOPA treatment on the NM-MRI signal.

273 ance, which was absent in control mice under l-DOPA treatment only.

274 ingly, repeated M2 stimulation combined with l-DOPA treatment produced an unanticipated improvement i

275 so assessed the ability of NM-MRI to predict L-DOPA treatment response in a subset of these patients

276 ctivity were lower in PD models than normal; L-DOPA treatment restored these properties.

277 l-Dopa treatment resulted in a partial but significant i

278 ns (6-OHDA) rendered dyskinetic with chronic L-DOPA treatment reveals a complex, Ras-GRF1 and pathway

279 Chronic L-DOPA treatment, which induced dyskinesia and aberrant

280 ptation of ChIs to dopamine loss and chronic L-DOPA treatment.

281 ns of genes aberrantly transcribed following l-DOPA treatment.

282 of motor control, which could be rescued by L-DOPA treatment.

283 dyskinesia-like effects of acute or chronic L-DOPA treatment.

284 ce with established dyskinesia after chronic L-DOPA treatment.

285 llowing sessions that were conducted without l-dopa treatment.

286 ability decreases toward normal values after L-DOPA treatment.

287 Ns did not change in PD models, it fell with L-DOPA treatment.

288 ed synaptic dopamine availability induced by L-DOPA treatment.

289 the striatopallidal knock-out in response to l-DOPA treatment.Our work shows, in a rodent model of PD

290 a from chronic L-3,4-dihydroxyphenylalanine (L-DOPA) treatment, but the physiological basis of these

291 L-DOPA treatments could partially improve the movement i

292 Glucose stimulation significantly enhances L-DOPA uptake, leading to increased DA release and GSIS

293 the accumulation of FosB produced by chronic L-DOPA was reduced in MSK1 knockout.

294 In this work, l-DOPA was used for the first time as a pro-angiogenic a

295 lood vessel formation when dexamethasone and l-DOPA were administered simultaneously.

296 acid and l-3,4-dihydroxyphenylalanine (i.e., l-DOPA), were attached to the shuttle.

297 ction of delay more strongly after receiving L-DOPA, whereas the opposite was detected for those with

298 catalyzes the conversion of l-tyrosine into l-DOPA, which is the rate-limiting step in the synthesis

299 vealed attenuated directed exploration under L-dopa, while neural signatures of exploration, exploita

300 of dSPNs exacerbated dyskinetic responses to L-DOPA, while stimulation of iSPNs inhibited these respo