ライフサイエンスコーパス: 6-OHDA

1 6-OHDA also decreased nuclear pCREB in dopaminergic neur

2 6-OHDA caused a loss of cells in the substantia nigra th

3 6-OHDA caused a transient and potent surge in isolated c

4 6-OHDA lesioning causes an increase of evoked striatal g

5 6-OHDA reduced uptake on the ipsilateral side relative t

6 6-OHDA significantly inhibited phosphorylation of GSK3be

7 6-OHDA, but not MPP+, significantly increased hallmarks

8 6-OHDA-induced splenic denervation also prevented ultras

9 lesion; and, Experiment 2 - exercise after a 6-OHDA lesion.

10 conducted: Experiment 1 - exercise before a 6-OHDA lesion; and, Experiment 2 - exercise after a 6-OH

11 dopamine neurons appear to be affected by a 6-OHDA insult and are potential targets for the neurotro

12 mphetamine-induced rotational asymmetry in a 6-OHDA animal model of PD.

13 results confirm that DFO is beneficial in a 6-OHDA model and demonstrate improvement in motor defici

14 sforming growth factor alpha (TGFalpha) in a 6-OHDA Parkinson's disease model when compared with naiv

15 and resulted in behavioral improvement in a 6-OHDA retrograde lesion model of PD.

16 splantation of Gpc4 hypomorphic cells into a 6-OHDA rat model for Parkinson's disease improved motor

17 We found that a 6-OHDA treatment of the OB produces olfactory deficits a

18 (2017) show that dopamine depletion using a 6-OHDA model causes a decrease in hyperdirect inputs fro

19 Here we show that neonatal but not adult 6-OHDA lesions result in a novel coupling of 5-HT2 recep

20 After 6-OHDA injection neuronal burst activity was enhanced, w

21 ve therapy when implemented before and after 6-OHDA hemiparkinsonism.

22 fer in normal mice and both before and after 6-OHDA lesion.

23 educed TUNEL in the lesioned nigra 2 d after 6-OHDA administration.

24 One day after 6-OHDA injection, HED (3.7-8.3 MBq) was injected intrave

25 Seven days after 6-OHDA lesion in the OB, we found that the integration o

26 elease provoked by dopamine deficiency after 6-OHDA-lesions or conditional KO of Nurr1.

27 wice daily for 14 days, beginning 24 h after 6-OHDA administration.

28 mine (5-HT) innervation remains intact after 6-OHDA lesions, suggesting that the 5-HT system may cont

29 matic suppression of neurodegeneration after 6-OHDA treatment.

30 pamine-mediated signaling is redundant after 6-OHDA lesions, 5-HT-mediated stimulation of the ERK1/2/

31 that GA has neuroprotective activity against 6-OHDA-induced oxidative stress via enhancement of cereb

32 TrkB activation also protected CGNs against 6-OHDA-induced damage.

33 Complete cytoprotection against 6-OHDA toxicity and restored MOC was achieved by combini

34 ctive and/or neuroreparative effects against 6-OHDA lesioning of the nigrostriatal DA pathway in an a

35 n the neuroprotective action of EGCG against 6-OHDA.

36 in vitro and in vivo neuroprotection against 6-OHDA toxicity in DA neurons, and preserved motor funct

37 d greatly diminished neuroprotection against 6-OHDA.

38 o provide functional neuroprotection against 6-OHDA; therefore, targeted activation of the endogenous

39 r tert-butylhydroquinone can protect against 6-OHDA in vitro.

40 ytes overexpressing Nrf2 can protect against 6-OHDA-induced damage in the living mouse.

41 s reduced microgliosis and protected against 6-OHDA neurotoxin-induced death of dopaminergic (DA) neu

42 s with Dexa were partially protected against 6-OHDA-induced dopaminergic neurodegeneration, which cor

43 signaling by Tat-Sab(KIM1) protected against 6-OHDA-induced oxidative stress, mitochondrial dysfuncti

44 ATF4 was also protective against 6-OHDA-induced death of cultured mouse ventral midbrain

45 ubstantia nigra pars compacta (SNpc) against 6-OHDA and MPTP.

46 the protective effect of G-substrate against 6-OHDA.

47 arget DNA sequence and MN9D survival against 6-OHDA toxicity.

48 on of abnormal involuntary movements (AIMs), 6-OHDA rats were injected with Daun02 in the dlBST previ

49 The two compounds alleviate 6-OHDA lesion-induced motor deficits.

50 tivation of TrkB in SH-SY5Y cells alleviated 6-OHDA-induced GSK3beta dephosphorylation (Ser9) and ame

51 Although 6-OHDA elicits phosphorylation of several kinases, downs

52 Although 6-OHDA lesions did not induce anhedonia in our model, th

53 eta dephosphorylation (Ser9) and ameliorated 6-OHDA neurotoxicity.

54 ted into PD model animals, aphakia mice, and 6-OHDA-lesioned rats, mDA NPs differentiated into mDA ne

55 D) animal models, reserpinized rat model and 6-OHDA induced unilaterally lesioned rat model.

56 Z were grafted to the striatum of normal and 6-OHDA lesioned adult rats.

57 teral 6-OHDA treated group; and the sham and 6-OHDA treated groups underwent respective surgeries.

58 tion of host NPCs to the transplantation and 6-OHDA was tracked by bromodeoxyuridine (BrdU) labeling.

59 plastic as exposure to neurotoxins, such as 6-OHDA or MPTP, that model certain aspects of Parkinson'

60 r showed that RTP801 and PD mimetics such as 6-OHDA trigger neuron death by suppressing activation of

61 studies revealed that FTY720 also attenuated 6-OHDA- or rotenone-induced toxicity in SH-SY5Y cells.

62 XENP345 also attenuated 6-OHDA-induced DA neuron toxicity in vitro.

63 cell line MN9D showed that leptin attenuated 6-OHDA-induced apoptotic markers, including caspase-9 an

64 mg/kg of minocycline beginning 3 days before 6-OHDA lesioning; (3) control: corresponding saline-trea

65 her IN DFO or saline (starting 4 days before 6-OHDA), and post-treated twice/wk for one month before

66 to three groups--control, sham and bilateral 6-OHDA treated group; and the sham and 6-OHDA treated gr

67 as a consequence of mTOR signaling blockade, 6-OHDA suppresses the phosphorylation and activation of

68 Furthermore, STN lesion completely blocked 6-OHDA- or D2 antagonist-induced GAD(67) mRNA increases

69 add153 was dramatically up-regulated by both 6-OHDA and MPP+.

70 kinases has been observed previously in both 6-OHDA-treated cells and degenerating human neurons, sup

71 The reduction of CYT-C by 6-OHDA, was extensive, occurred within minutes, preceded

72 ulated kinases (ERK1/2) activities caused by 6-OHDA toxicity.

73 but does not further elevate death caused by 6-OHDA.

74 The H2O2 generated by 6-OHDA contributed toward the loss of anaerobic glycolys

75 appears to underlie neuron death induced by 6-OHDA.

76 nd rats acutely or progressively lesioned by 6-OHDA injected into the medial forebrain bundle or ST,

77 tive against depression of activity level by 6-OHDA than the non-recycling antioxidant, TEMPOL, in a

78 the degeneration of dopaminergic neurons by 6-OHDA and may prove useful in the treatment of Parkinso

79 At similar concentrations, 6-OHDA readily altered the valence state of iron [Fe(III

80 In contrast, 6-OHDA alters the redox of the cytochromes, resulting in

81 F4 enhanced cell death in response to either 6-OHDA or MPP+.

82 As expected, 6-OHDA induced a severe loss of DA, an increase in ME, a

83 In another experiment, 6-OHDA lesions were applied to transgenic mice with a ce

84 ling in Neuro-2a and SH-SY5Y cells following 6-OHDA treatment, and contributes to oxidopamine-mediate

85 was essential for neuroprotection following 6-OHDA toxicity.

86 s cathecolamine-producing SH-SY5Y cells from 6-OHDA-induced reactive oxygen species formation, caspas

87 that torsins seem to protect DA neurons from 6-OHDA through downregulating protein levels of the dopa

88 s ventral midbrain dopaminergic neurons from 6-OHDA, MPP+, or alphaSYN.

89 rylated Akt and protected A9 DA neurons from 6-OHDA-induced toxicity.

90 density, and neuronal volume resulting from 6-OHDA lesion differed between regions, with the SNpc ex

91 Furthermore, 6-OHDA decreased the expression of cyclin D1, a substrat

92 The highest 6-OHDA dose of 100 mg/kg caused severe cardiac denervati

93 nism-inducing neurotoxins 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium (MPP+) in a dopa

94 aminergic neuronal toxins 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium (MPP+).

95 ing an oxidative stressor 6-hydroxydopamine (6-OHDA) and a proteasome inhibitor MG-132.

96 ed in the pharmacological 6-hydroxydopamine (6-OHDA) animal models of Parkinson's disease include spo

97 Rats lesioned with 6-hydroxydopamine (6-OHDA) as neonates exhibit behavioral and neurochemical

98 ability to the neurotoxin 6-hydroxydopamine (6-OHDA) both in vitro and in vivo.

99 ranscriptional level in a 6-hydroxydopamine (6-OHDA) cellular model of PD.

100 We previously found that 6-hydroxydopamine (6-OHDA) elicits sustained extracellular signal-regulated

101 The neurotoxin, 6-hydroxydopamine (6-OHDA) has been implicated in the neurodegenerative pro

102 euronal loss by injecting 6-hydroxydopamine (6-OHDA) in the dorsal GL or in the right substantia nigr

103 cle containing or lacking 6-hydroxydopamine (6-OHDA) in the ipsilateral medial forebrain bundle (MFB)

104 e that rats lesioned with 6-hydroxydopamine (6-OHDA) in the medial forebrain bundle display significa

105 catecholamine neurotoxin 6-hydroxydopamine (6-OHDA) induced a selective depletion of norepinephrine

106 n vivo effects of BMP7 on 6-hydroxydopamine (6-OHDA) induced lesioning of midbrain DA neurons.

107 Six weeks after 6-hydroxydopamine (6-OHDA) infusion into the medial forebrain bundle, rats

108 Animals previously given 6-hydroxydopamine (6-OHDA) injections into the ascending DA pathways had gr

109 he basal forebrain and/or 6-hydroxydopamine (6-OHDA) into the caudate nucleus, respectively, modeling

110 a unilateral injection of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle, while sham sur

111 report that injections of 6-hydroxydopamine (6-OHDA) into the mouse striatum cause a local increase i

112 6-Hydroxydopamine (6-OHDA) is an oxidative neurotoxin used to injure catech

113 While 6-hydroxydopamine (6-OHDA) is often used in animal models of DA neuron dege

114 ne system by injection of 6-hydroxydopamine (6-OHDA) lead to abnormal neuronal activity in the basal

115 against an intrastriatal 6-hydroxydopamine (6-OHDA) lesion in the common marmoset.

116 ine-induced akinesia, rat 6-hydroxydopamine (6-OHDA) lesion model of drug-induced rotation, and MPTP-

117 ced akinesia, and the rat 6-hydroxydopamine (6-OHDA) lesion model of drug-induced rotation.

118 unilateral intrastriatal 6-hydroxydopamine (6-OHDA) lesion model of PD on the number, morphology, an

119 exploited the unilateral 6-hydroxydopamine (6-OHDA) lesion model to assess the effect of minocycline

120 unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) lesion model using optogenetic and pharmacologic

121 epsy in mouse and the rat 6-hydroxydopamine (6-OHDA) lesion model.

122 ms of parkinsonism in the 6-hydroxydopamine (6-OHDA) lesion rat.

123 rats following unilateral 6-hydroxydopamine (6-OHDA) lesion using an ultrafast opsin (Chronos).

124 duced rotations caused by 6-hydroxydopamine (6-OHDA) lesion.

125 progression of a striatal 6-hydroxydopamine (6-OHDA) lesion.

126 One model was 6-hydroxydopamine (6-OHDA) lesioning and the other was direct gene transfer

127 ent induced by unilateral 6-hydroxydopamine (6-OHDA) lesions in the medial forebrain bundle.

128 d, we tested animals with 6-hydroxydopamine (6-OHDA) lesions of the PL and IL mPFC on three tests of

129 Nigral 6-hydroxydopamine (6-OHDA) lesions or repeated D2-class antagonist injectio

130 m rodents with unilateral 6-hydroxydopamine (6-OHDA) lesions.

131 in a mouse intrastriatal 6-hydroxydopamine (6-OHDA) model of hemiparkinsonism.

132 und to be protective in a 6-hydroxydopamine (6-OHDA) model of the disease.

133 levels in the unilateral 6-hydroxydopamine (6-OHDA) mouse model of dopaminergic cell death.

134 levels in mice receiving 6-hydroxydopamine (6-OHDA) or rotenone to simulate PD.

135 neurodegeneration in the 6-hydroxydopamine (6-OHDA) PD model.

136 was neuroprotective in a 6-hydroxydopamine (6-OHDA) rat model of parkinsonism.

137 motor asymmetry in adult, 6-hydroxydopamine (6-OHDA) rats.

138 th was investigated using 6-hydroxydopamine (6-OHDA) to abolish early sympathetic innervation of the

139 e dopaminergic (DA) toxin 6-hydroxydopamine (6-OHDA) to model PD and explore the protective effect an

140 opamine (DA) neurons from 6-hydroxydopamine (6-OHDA) toxicity.

141 increased in response to 6-hydroxydopamine (6-OHDA) treatment.

142 unilateral, intrastriatal 6-hydroxydopamine (6-OHDA) was used to investigate how dopamine depletion a

143 then exposed to dopamine, 6-hydroxydopamine (6-OHDA), 4-hydroxy-2-nonenal (HNE), or H2O2, agents that

144 tion after treatment with 6-hydroxydopamine (6-OHDA), a neurotoxin commonly used to model PD.

145 6-Hydroxydopamine (6-OHDA), a PD mimetic, is widely used to model this neur

146 e shown that injection of 6-hydroxydopamine (6-OHDA), a toxin devoid of saporin, also damaged NTS cat

147 such as dopamine (DA) and 6-hydroxydopamine (6-OHDA), and resulting in oxidative stress.

148 treatment with neurotoxin 6-hydroxydopamine (6-OHDA), leading to the biosynthesis of PGE2 and upregul

149 ns of DA neurons by using 6-hydroxydopamine (6-OHDA), to ascertain whether N/OFQ and the N/OFQ recept

150 nd nigral DA cell loss in 6-hydroxydopamine (6-OHDA)-induced and rotenone-induced rat models of PD.

151 ting systems arises after 6-hydroxydopamine (6-OHDA)-induced dopamine depletion, highlighting the cen

152 n in rats with unilateral 6-hydroxydopamine (6-OHDA)-induced lesions of nigrostriatal dopamine (DA) n

153 e rotational behaviour in 6-hydroxydopamine (6-OHDA)-lesioned rats and to potentiate the effects of l

154 recently reported that in 6-hydroxydopamine (6-OHDA)-lesioned striatum, norepinephrine transporter (N

155 markably, after a partial 6-hydroxydopamine (6-OHDA)-mediated DA depletion ( approximately 70% in dor

156 in the hemi-Parkinsonian 6-hydroxydopamine (6-OHDA)-treated rat and 2) locomotion in the reserpine-t

157 nduced by the PD-mimetic, 6-hydroxydopamine (6-OHDA).

158 nfused ipsilaterally with 6-hydroxydopamine (6-OHDA).

159 the oxidative neurotoxin 6-hydroxydopamine (6-OHDA).

160 cally with the neurotoxin 6-hydroxydopamine (6-OHDA).

161 trastriatal injections of 6-hydroxydopamine (6-OHDA).

162 laminergic ROS generator, 6-hydroxydopamine (6-OHDA).

163 brain bundle injection of 6-hydroxydopamine (6-OHDA).

164 idative stress induced by 6-hydroxydopamine (6-OHDA).

165 renoceptor antagonist) or 6-hydroxydopamine (6-OHDA, an agent that induces chemical sympathectomy) ha

166 lesioned as neonates with 6-hydroxydopamine (6-OHDA, intracisternally) on the third postnatal day.

167 idative stress induced by 6-hydroxydopamine (6-OHDA; 8 mug/2 muL) injected into the medial forebrain

168 o in producing potent rotational activity in 6-OHDA lesioned rats.

169 In addition, in 6-OHDA-lesioned rats beta-band oscillatory activity was

170 e for death in our cellular PD models and in 6-OHDA-treated cultured sympathetic neurons in that its

171 ssion is altered concomitant with changes in 6-OHDA sensitivity.

172 the survival factor Bcl-2 were decreased in 6-OHDA-treated cells, but message levels of genes lackin

173 plasma levels, or Cav1.3 LTCC deficiency in 6-OHDA-treated male mice.

174 ther, compound 49 displayed oral efficacy in 6-OHDA lesioned rat model of Parkinson diseases.

175 physiological tonic, single-spike firing in 6-OHDA rats in vivo.

176 st striatum to produce motor improvements in 6-OHDA rats, a Parkinson's disease model.

177 ress-responsive phosphatase, was involved in 6-OHDA-induced GSK3beta dephosphorylation (Ser9).

178 d spatial patterns of ERK phosphorylation in 6-OHDA-treated cells and in human postmortem tissues rep

179 LD, which display a substantial reduction in 6-OHDA-induced neurotoxicity, as shown by increased surv

180 t ERK1/2 activation was confirmed in vivo in 6-OHDA-lesioned animals treated systemically with SKF383

181 ic BE(2)-M17 cells against toxins, including 6-OHDA and MG-132 (carbobenzoxy-L-leucyl- L-leucyl-L-leu

182 n the etiology of 6-hydroxydopamine-induced (6-OHDA) oxidative stress, mitochondrial dysfunction, and

183 PRX2 inhibited 6-OHDA-induced ASK1 activation by modulating the redox s

184 avated degeneration induced by intrastriatal 6-OHDA in WT mice.

185 These findings indicate that intrastriatal 6-OHDA lesion differentially affects dopaminergic neuron

186 inergic markers in response to intrastriatal 6-OHDA administration compared with wild-type (WT) litte

187 either the effects of PAR-1 nor TPC on later 6-OHDA-induced behavioral deficits appeared to be mediat

188 s with unilateral 6-hydroxydopamine lesions (6-OHDA) rendered dyskinetic with chronic L-DOPA treatmen

189 c PC12 cells was triggered by the PD mimetic 6-OHDA.

190 In isolated mitochondria, 6-OHDA had negligible effects on complex I, inhibited co

191 ven a single injection of vehicle or 100 mug 6-OHDA into the right lateral ventricle.

192 Neonatal 6-OHDA lesions actually give rise to a 5-HT axonal hyper

193 ion of direct pathway neurons after neonatal 6-OHDA lesions involves coupling of 5-HT2 receptors to t

194 e nigrostriatal region induced by neurotoxin 6-OHDA, a Parkinsonian animal model.

195 The neurotoxin 6-OHDA was injected into the medial forebrain bundle (MF

196 Five or 21 d after nigral 6-OHDA injections or after 3, 7, or 21 d of D2 antagonis

197 Neither PRZ nor 6-OHDA affected the expression of cytokines, growth fact

198 The ability of 6-OHDA to maintain oxidized cytochrome c (CYT-C-OX) in i

199 essential for COX-2-dependent activation of 6-OHDA oxidation, oxygen radical production, oxidative s

200 ere associated with enhanced cytotoxicity of 6-OHDA in stably transfected PC12 cells.

201 h group was administered a different dose of 6-OHDA: 0 (controls), 7, 11, 15, 22, and 100 mg/kg intra

202 Comparing values for all doses of 6-OHDA, HED retention had a strong linear correlation wi

203 ew studies that have examined the effects of 6-OHDA in older animals.

204 ed to elucidate the toxicological effects of 6-OHDA on energy metabolism in neuroblastoma (N-2A) cell

205 KO mice exhibit attenuated toxic effects of 6-OHDA on nigral dopaminergic cell counts, striatal dopa

206 derwent unilateral intrastriatal infusion of 6-OHDA (12.5mug).

207 , minimal cytotoxicity, potent inhibition of 6-OHDA-induced mitochondrial membrane potential dissipat

208 with cAMP several hours after initiation of 6-OHDA injury.

209 We performed unilateral injections of 6-OHDA into the striatum of C57Bl/6 mice to model hemi-P

210 lowed by local administration of 9 microg of 6-OHDA into the left medial forebrain bundle.

211 Indeed, in a lower-dose model of 6-OHDA (5 microg), PAR-4 preconditioning significantly i

212 hose of fully dopamine (DA)-depleted MSNs of 6-OHDA-treated mice, together with the beneficial effect

213 he cytoplasm and decreased in the nucleus of 6-OHDA-treated cells.

214 Finally, co-oxidation of 6-OHDA by COX-2 triggered production of superoxide radic

215 eme-reconstituted COX-2 induced oxidation of 6-OHDA in the course of its peroxidase (H(2)O(2)-depende

216 e stress is restricted to the acute phase of 6-OHDA neurotoxicity.

217 de radicals critical for both propagation of 6-OHDA oxidation and induction of oxidative stress in CO

218 activity, with rapid recovery as a result of 6-OHDA recycling CYT-C-OX to CYT-C-RED.

219 The toxicity of 6-OHDA corresponds to the total collapse of anaerobic/ae

220 The toxicity of 6-OHDA paralleled the loss of mitochondrial oxygen (O2)

221 in protecting neuronal PC12 from toxicity of 6-OHDA.

222 d neuroprotection, they had little effect on 6-OHDA-induced GSK3beta activation.

223 fects of subthalamic nucleus (STN) lesion on 6-OHDA- or repeated D2 antagonist-induced changes in GP

224 UPR proteins, PERK and eIF2 alpha, but only 6-OHDA increased phosphorylation of c-Jun.

225 exposure to SAP, targeted SAP conjugates, or 6-OHDA.

226 (SH-SY5Y) against apoptosis induced by DA or 6-OHDA, but not by H(2)O(2) or rotenone.

227 nst neuronal injuries induced by ischemia or 6-OHDA through the inhibition of apoptosis.

228 rtantly, in vivo studies using MPTP, LPS, or 6-OHDA models revealed a greater attenuation of neuroinf

229 esions (DL) fell more frequently than SAP or 6-OHDA rats.

230 rs (lithium, TDZD-8, and L803-mts) prevented 6-OHDA-induced cleavage of caspase-3 and poly(ADP-ribose

231 LRRK2 ultimately promoted 6-OHDA-induced cell death via positive modulation of HDA

232 was also observed in a mild progressive rat 6-OHDA-lesion model.

233 In male Sprague-Dawley rats 6-OHDA (n = 12) or vehicle (n = 10) was bilaterally inje

234 Six hours later, animals received 6-OHDA (4 mug) into the same site.

235 lative to controls in rats that had received 6-OHDA lesions and deposition of FG in the Acb core as c

236 G-substrate reduced 6-OHDA-mediated protein phosphatase 2A (PP2A) activation

237 However, selective 6-OHDA lesions of the dorsolateral striatum also had a p

238 nd lateral motor part, and whether selective 6-OHDA-induced lesions of the dorsolateral striatum, the

239 Similarly, COX-2 was able to stimulate 6-OHDA oxidation during its peroxidase- and cyclooxygena

240 udy, male Fischer 344 rats received striatal 6-OHDA lesions followed 1 week later by an intraventricu

241 We demonstrate here that 6-OHDA evoked endoplasmic reticulum (ER) stress, which w

242 In vitro studies showed that 6-OHDA induced JNK translocation to the mitochondria and

243 The results showed that 6-OHDA significantly reduced the passive avoidance memor

244 Collectively, these data suggest that 6-OHDA induced JNK translocation to the mitochondria and

245 The 6-OHDA incubation caused Nur77 translocation from the nu

246 The 6-OHDA treatments had no effect on horizontal activity o

247 The 6-OHDA treatments led to significant decreases in both p

248 The 6-OHDA-lesioned rats that received repeated intravenous

249 The 6-OHDA-promoted cytotoxicity was largely blocked by TG4-

250 minocycline treatment immediately after the 6-OHDA administration rescued neither TH(+) interneuron

251 ctions, and that NPC implantation before the 6-OHDA insult can create a host microenvironment conduci

252 and were significantly less impaired in the 6-OHDA model of Parkinson's disease.

253 ne (Dexa) into the CD163+ macrophages in the 6-OHDA PD model.

254 ring and alleviates motor impairments in the 6-OHDA rat model of Parkinson's disease.

255 on, DNA damage, and neuroinflammation in the 6-OHDA rat model of PD, suggesting that SRY directly con

256 gnificantly attenuated motor deficits in the 6-OHDA-hemilesioned rat model of PD.

257 and their projections to the striatum in the 6-OHDA-lesioned hemisphere.

258 into the dopamine-denervated striatum of the 6-OHDA-lesioned rat, sustained expression of each enzyme

259 al prostaglandin E synthase-1 suppressed the 6-OHDA-triggered PGE2 production in these cells.

260 It was found that the 6-OHDA lesion group failed to exhibit behavioral sensiti

261 ated to the loss of motor control due to the 6-OHDA lesion.

262 Thus, 6-OHDA is capable of triggering multiple pathways associ

263 observed in primary human neurons exposed to 6-OHDA or HNE.

264 y and sufficient for increased resistance to 6-OHDA in differentiated neuroblastoma cells, and that C

265 d sex differences in the brain's response to 6-OHDA, and imply that compensatory or neuroprotective m

266 blastoma cells display higher sensitivity to 6-OHDA than differentiated cells.

267 on of L-DOPA to adult rats with a unilateral 6-OHDA lesion of dopamine neurons on GABA release in the

268 ent brain sections of mice with a unilateral 6-OHDA lesion of the medial forebrain bundle were chosen

269 silateral rotation in rats with a unilateral 6-OHDA lesion of the nigro-striatal pathway.

270 for PAR-1 and PAR-4 3 days before unilateral 6-OHDA administration (10 microg into the medial forebra

271 hat were rendered parkinsonian by unilateral 6-OHDA injection.

272 were rendered hemiparkinsonian by unilateral 6-OHDA lesions and primed with the D1R agonist SKF81297

273 Similarly, neither unilateral 6-OHDA lesions of nigrostriatal axons nor the dorsal nor

274 nduced involuntary movements than unilateral 6-OHDA-lesioned RGS9+/+ mice, albeit the rotational beha

275 We also find that unilateral 6-OHDA-lesioned RGS9-/- mice are more susceptible to L-d

276 ffects of l-DOPA treatment in the unilateral 6-OHDA lesioned mouse model of Parkinson's disease.

277 ipsilateral turning in rats with unilateral 6-OHDA nigrostriatal lesion and increased withdrawal lat

278 In unilaterally 6-OHDA-lesioned rats with LID, we show that the time cou

279 ed BMP7 pretreatment, as compared to vehicle/6-OHDA controls, had a significant reduction in methamph

280 assessments of a rodent model of PD, wherein 6-OHDA was injected into the dorsolateral striatum of bo

281 The mechanism by which 6-OHDA and RTP801 induce neuron death appears to involve

282 n, a marker for astrocytes, in the NTS while 6-OHDA did not.

283 ts that have been chemically denervated with 6-OHDA, suggesting that HED retention is a good surrogat

284 t-pathway MSNs after dopamine depletion with 6-OHDA.

285 Experiment 2, rats were first injected with 6-OHDA and were then randomly assigned into one of the t

286 erimental conditions rats were injected with 6-OHDA into the right medial forebrain bundle.

287 effects of a bilateral, partial lesion with 6-OHDA in young (4 months), middle-aged (14 months), and

288 of TAAR1 KO mice unilaterally lesioned with 6-OHDA in the medial forebrain bundle resulted in more p

289 arkinsonian mice (unilaterally lesioned with 6-OHDA) were treated daily for 3 weeks with a low dose o

290 y 2-fold (p < 0.05) in animals lesioned with 6-OHDA, compared with animals treated only with 6-OHDA i

291 HDA, compared with animals treated only with 6-OHDA into the nigrostriatal pathway.

292 c neuronal cell lines (B65 and SH-SY5Y) with 6-OHDA resulted in repression of basal CRE transactivati

293 vitro studies with PC-12 cells treated with 6-OHDA and rotenone, respectively.

294 on of cleaved caspase-3 in mice treated with 6-OHDA or rotenone.

295 nergic ventral midbrain neurons treated with 6-OHDA, 1-methyl-4-phenylpyridinium (MPP+), or alpha-syn

296 sm to the nucleus of PC12 cells treated with 6-OHDA, but in vivo, TEMPOL/PNA maintains redox-active b

297 Treatment with 6-OHDA also induced a large number of genes involved in

298 were euthanized 14 days after treatment with 6-OHDA and brains were stained with a tyrosine hydroxyla

299 After treatment with 6-OHDA or MPP+, parkin protein levels fall, despite an i

300 XENP345/6-OHDA rats displayed attenuated amphetamine-induced rot