ライフサイエンスコーパス: L-dopa

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

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

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

4 denervation and pulsatile administration of L-DOPA.

5 while maintaining the therapeutic effect of L-DOPA.

6 akly dyskinetic animals after treatment with L-DOPA.

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

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

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

10 out compromising the therapeutic efficacy of L-DOPA.

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

12 gical restoration of dopamine synthesis with l-dopa.

13 g dyskinesias, warranting discontinuation of l-DOPA.

14 s and indicate that this can be modulated by L-DOPA.

15 no change was observed after treatment with L-DOPA.

16 down cells when incubated with the substrate l-DOPA.

17 ursors and metabolites as norepinephrine and l-DOPA.

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

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

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

21 6-(18)F-fluoro-L-dopa ((18)F-FDOPA) has proven to be a useful radiophar

22 ll as the prognostic power of 6-(18)F-fluoro-l-dopa ((18)F-FDOPA) PET for differentiating RPBM from L

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

24 nal(+)/(+) and Gnal(+)/(-) mice after a 10-d L-DOPA (20 mg/kg) treatment.

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

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

27 norepinephrine, 3,4-dihydroxy-phenylalanine (L-DOPA), 3,4-dihydroxyphenylacetic acid (DOPAC), methyld

28 groups, and allows access to 6-[(18)F]fluoro-L-DOPA, 6-[(18)F]fluoro-m-tyrosine, and the translocator

29 We found that (1) a 50% reduced dose of L-dopa (7.5 mg/kg) combined with acupuncture showed an i

30 Treatment with l-DOPA, a DA precursor, improved overall retinal and vis

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

32 In the dopamine (DA)-denervated striatum, L-DOPA activates DA D(1) receptor(D(1)R) signaling, incl

33 nly, and that (2) the combination treatment (L-dopa +acupuncture) was significantly superior in reduc

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

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

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

37 pressed more severe dyskinesia compared with L-DOPA alone over time.

38 take in the DMI + L-DOPA group compared with L-DOPA-alone group in lesioned striatum.

39 L-Dopa also enhanced demethylated PP2A amounts in the li

40 rkinson's disease are commonly treated using l-DOPA although long-term treatment usually causes debil

41 -dopa on motor function with reduced dose of L-dopa and alleviating LID by normalising neurochemical

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

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

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

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

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

47 lts indicate that the combination of chronic L-DOPA and NET-mediated DA reuptake in lesioned nigrostr

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

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

50 ats showed greater dyskinesia in response to l-DOPA and SKF81297 after repeated injections.

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

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

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

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

55 dependent of whether patients were ON or OFF l-DOPA, and were associated with increases in subthalami

56 K1/2 in DMI + L-DOPA group compared with the L-DOPA- and DMI-alone groups.

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

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

59 hod, employing l-3,4-dihydroxyphenylalanine (L-DOPA) as a reducing/capping reagent, for the synthesis

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

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

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

63 phenolic that may have beneficial effects in L-DOPA-based treatment of Parkinson patients by inhibiti

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

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

66 n by excessive extracellular DA derived from L-DOPA, but potential involvement of DA reuptake in LID

67 Here we show that L-dopa can alter basal ganglia activity and produce LID

68 tant mice exhibit an exaggerated response to l-DOPA compared with control mice, suggesting that prese

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

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

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

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

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

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

75 arious organic and inorganic species such as l-dopa, dopac, iron(II), and iodide are measured by bare

76 lerated, although weight loss was common and l-dopa dose failures occurred in a single patient.

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

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

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

80 With a high degree of denervation, l-dopa enhanced another aberrant signal, this time in th

81 or the selective and precise analysis of DA, l-Dopa, EP and NE in pharmaceutical formulations, urine

82 9)M, 3.96x10(-10)M and 3.54x10(-10)M for DA, l-Dopa, EP and NE respectively.

83 atecholamines viz., dopamine (DA), levodopa (l-Dopa), epinephrine (EP) and norepinephrine (NE) using

84 study, pigments produced with L-dopa, methyl-L-dopa, epinephrine, and norepinephrine precursors are c

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

86 dopamine agonist and 95 with l-dopa (median l-dopa equivalent dose 300 mg).

87 owerful clinical option as an alternative to L-DOPA, especially in the early stages of the disease, b

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

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

90 By contrast, L-DOPA failed to normalize fast-spiking interneuron acti

91 Surprisingly, while L-DOPA fails to restore these critical synaptic alterati

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

93 ly used in treating these disorders, such as L-DOPA for Parkinson's disease, methylphenidate for atte

94 We argue that the need of l-DOPA for successful reproduction has driven D. sechell

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

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

97 s of protected forms of (R)-beta(3)-DOPA and L-DOPA from the same aziridine, the former by SmI2-media

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

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

100 ediated inhibition of DA uptake in the DMI + L-DOPA group compared with L-DOPA-alone group in lesione

101 ent groups, with increased ppERK1/2 in DMI + L-DOPA group compared with the L-DOPA- and DMI-alone gro

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

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

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

105 The symptoms of parkinsonism improved with l-DOPA; however, nearly all patients experienced early m

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

107 This effect is due to L-DOPA impairing the ability to update belief in respons

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

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

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

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

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

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

114 However, d-DOPA coexisting with l-DOPA in the incubation solution remained intact.

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

116 transferase (COMT)-mediated O-methylation of L-DOPA in vitro, only (+)-catechin exerts a significant

117 A clinical trial of levodopa (L-DOPA) in AS is ongoing, although the underlying ration

118 The dopamine precursor levodopa (L-DOPA) increased the task-based learning rate and task

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

120 inergic function (dihydroxy-L-phenylalanine; L-DOPA) increases an optimism bias.

121 ression of FosB, the immediate early gene of L-dopa induced dyskinesia (LID), was mitigated in the st

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

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

124 3,4-Dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia (LID) is a debilitating side

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

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

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

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

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

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

131 es demonstrate that, in D1R-expressing MSNs, l-DOPA-induced activation of ERK and mTORC1 requires DAR

132 emonstrate that this protein is required for l-DOPA-induced activation of the extracellular signal-re

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

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

135 tating abnormal involuntary movements termed L-DOPA-induced dyskinesia (LID), a clinically significan

136 L-DOPA-induced dyskinesia (LID), a detrimental consequen

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

138 amine D(1) receptor (D1R) is associated with L-DOPA-induced dyskinesia (LID), a major complication of

139 hophysiology in Parkinson's disease (PD) and L-DOPA-induced dyskinesia (LID).

140 ting side effects, known in their complex as L-DOPA-induced dyskinesia (LID).

141 long-term beneficial effects are hindered by L-DOPA-induced dyskinesia (LID).

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

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

144 ated that its overexpression plays a role in L-dopa-induced dyskinesia and in drug addiction.

145 endent protein kinase on DARPP-32 attenuates l-DOPA-induced dyskinesia and reduces the concomitant ac

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

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

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

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

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

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

152 genesis of Parkinson's disease, also affects L-DOPA-induced dyskinesia.

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

154 in later stages, treatment is complicated by L-dopa-induced dyskinesias (LID).

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

156 rstand how these striatal circuits change in l-DOPA-induced dyskinesias (LIDs).

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

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

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

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

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

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

163 may represent a novel strategy to counteract L-DOPA-induced dyskinesias.

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

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

166 In contrast, the persistence of L-DOPA-induced ERK activation in Gnal(+)/(-) mice suppor

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

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

169 oamphetamine increased both the baseline and l-dopa-induced normal ambulatory and dyskinetic movement

170 tromedial striatum, +/-8-OH-DPAT potentiated l-DOPA-induced pERK; in the motor cortex, +/-8-OH-DPAT p

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

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

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

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

175 involving methylation-dependent pathways in L-dopa induces PP2A hypomethylation and increases Tau ph

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

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

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

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 Levodopa (L-DOPA) is widely used for symptomatic management in Par

182 kinsonian drug l-3,4-dihydroxyphenylalanine (l-DOPA), is accompanied by activation of cAMP signaling

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

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

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

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

187 ion administration of the dopamine precursor L-dopa makes extinction memories context-independent, th

188 treated with a dopamine agonist and 95 with l-dopa (median l-dopa equivalent dose 300 mg).

189 In the current study, pigments produced with L-dopa, methyl-L-dopa, epinephrine, and norepinephrine p

190 d (quercetin), for their ability to modulate L-DOPA methylation and to protect against oxidative hipp

191 e stronger in vivo effect of (+)-catechin on L-DOPA methylation compared to the other dietary compoun

192 -catechin exerts a significant inhibition of L-DOPA methylation in both peripheral compartment and st

193 reatment of Parkinson patients by inhibiting L-DOPA methylation plus reducing oxidative neurodegenera

194 gallate, a tea polyphenol, not only inhibits L-DOPA methylation, but also protects against oxidative

195 L-DOPA normalizes these dynamics except at low-gamma, li

196 regulation is critical for the activation by L-DOPA of D(1)R-stimulated cAMP/PKA but not ERK signalin

197 te that acupuncture enhances the benefits of L-dopa on motor function with reduced dose of L-dopa and

198 The effect of L-dopa on PP2A and p-Tau was exacerbated in cells expose

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

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

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

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

203 e in vivo, caused by one injection of either l-DOPA or cocaine, induced adult-like, non-desensitizing

204 Vesicular content was markedly increased by L-DOPA or decreased by reserpine in a time-dependent man

205 r cortex, +/-8-OH-DPAT potentiated pERK with l-DOPA or SKF81297.

206 OH-DPAT on pERK density in rats treated with l-DOPA or the D1 receptor agonist SKF81297.

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

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

209 coating, poly(butadiene-maleic anhydride-co-L-DOPA) (PBMAD), to non-bioadhesive nanospheres resulted

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

211 l-DOPA present in morinda additionally increases the siz

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

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

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

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

216 L-dopa remains the mainstay treatment for Parkinson's di

217 Although L-3,4-dihydroxyphenylalanine (L-DOPA) remains the reference treatment of Parkinson's d

218 Dopamine replacement with levodopa (L-DOPA) represents the mainstay of Parkinson's disease (

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

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

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

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

225 In the folate-deficient mouse model, L-dopa resulted in a marked depletion of SAM and an incr

226 minergic neurons, and in wild-type mice that l-dopa results in a reduced SAM/SAH ratio that is associ

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

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

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

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

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

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

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

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

235 uction was similar between acute and chronic l-DOPA, SKF81297 caused the largest increase in striatal

236 opamine and primed with a chronic regimen of l-DOPA, SKF81297 or their vehicles.

237 SCH23390 or their vehicles, and second with l-DOPA, SKF81297 or their vehicles.

238 In Gnal(+)/(-) mice, the lesion-induced L-DOPA stimulation of cAMP/PKA-mediated phosphorylation

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

240 elationship was significantly stronger under L-Dopa than under Placebo, suggesting that the impact of

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

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

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

244 s that may inform ongoing clinical trials of L-DOPA therapy in patients with AS.

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

246 L-DOPA therapy normalized all of these effects except th

247 Simulation of l-dopa therapy reduced the aberrant D2 signal.

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 etic profile or antiparkinsonian efficacy of L-DOPA therapy.

251 ck normalization of spike activity following l-DOPA therapy.

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

253 ganglia circuits, which can be normalized by L-DOPA therapy.

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

255 Levodopa (L-dopa) therapy in PD patients has been shown to cause a

256 cle for the majority of patients who rely on L-DOPA to alleviate PD-related motor symptoms.

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

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

261 o dyskinetic effects in lesioned rats, DMI + L-DOPA-treated rats gradually expressed more severe dysk

262 omparable to mice given the standard dose of L-dopa treatment (15 mg/kg) only, and that (2) the combi

263 nkey model of PD; (2) to investigate whether l-dopa treatment alleviates sleep disorders; and (3) to

264 Remarkably, L-DOPA treatment almost entirely reversed the depletion-

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

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

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

268 ed dyskinesia (LID), a major complication of L-DOPA treatment in Parkinson's disease (PD).

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

270 However, long-term L-DOPA treatment is complicated by eventual debilitating

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

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

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

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

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

276 kinesia, but maintained motor improvement on L-DOPA treatment, suggesting a therapeutic benefit for R

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

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

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

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

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

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

283 he substantia nigra compared to the standard L-dopa treatment.

284 n mice are correlated with LID after chronic L-DOPA treatment.

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

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

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

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

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

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

291 reducing AIM scores when equivalent doses of L-dopa were used.

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

293 they received one of the following: placebo, L-DOPA (which increases dopamine levels in the brain), o

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

295 e advanced stages of PD, in conjunction with L-DOPA, which is used in this context at lower dosages,

296 potentiometry) toward two different species; l-dopa, which shows fast electron transfer on Pt, and ca

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

298 ral benefits of novel combination therapy of L-dopa with acupuncture on Parkinson's disease, and its

299 Hence, we hypothesised that combining L-dopa with acupuncture would have a behavioural benefit

300 ydroxydopamine hemilesioned rats primed with L-DOPA, without causing primary hypolocomotive effects.