ライフサイエンスコーパス: OHDA

1 6-OHDA also decreased nuclear pCREB in dopaminergic neuron

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

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

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

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

6 6-OHDA significantly inhibited phosphorylation of GSK3beta

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

8 6-OHDA-induced splenic denervation also prevented ultrasou

9 hetamine-induced rotational asymmetry in a 6-OHDA animal model of PD.

10 opamine neurons appear to be affected by a 6-OHDA insult and are potential targets for the neurotroph

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

12 onducted: Experiment 1 - exercise before a 6-OHDA lesion; and, Experiment 2 - exercise after a 6-OHDA

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

14 2017) show that dopamine depletion using a 6-OHDA model causes a decrease in hyperdirect inputs from

15 orming growth factor alpha (TGFalpha) in a 6-OHDA Parkinson's disease model when compared with naive

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

17 nd resulted in behavioral improvement in a 6-OHDA retrograde lesion model of PD.

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

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

20 ce daily for 14 days, beginning 24 h after 6-OHDA administration.

21 uced TUNEL in the lesioned nigra 2 d after 6-OHDA administration.

22 therapy when implemented before and after 6-OHDA hemiparkinsonism.

23 After 6-OHDA injection neuronal burst activity was enhanced, whi

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

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

26 r in normal mice and both before and after 6-OHDA lesion.

27 mine-mediated signaling is redundant after 6-OHDA lesions, 5-HT-mediated stimulation of the ERK1/2/MA

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

29 tic suppression of neurodegeneration after 6-OHDA treatment.

30 ease provoked by dopamine deficiency after 6-OHDA-lesions or conditional KO of Nurr1.

31 stantia nigra pars compacta (SNpc) against 6-OHDA and MPTP.

32 tert-butylhydroquinone can protect against 6-OHDA in vitro.

33 ive and/or neuroreparative effects against 6-OHDA lesioning of the nigrostriatal DA pathway in an ani

34 reduced microgliosis and protected against 6-OHDA neurotoxin-induced death of dopaminergic (DA) neuro

35 Complete cytoprotection against 6-OHDA toxicity and restored MOC was achieved by combining

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

37 get DNA sequence and MN9D survival against 6-OHDA toxicity.

38 es overexpressing Nrf2 can protect against 6-OHDA-induced damage in the living mouse.

39 rkB activation also protected CGNs against 6-OHDA-induced damage.

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

41 with Dexa were partially protected against 6-OHDA-induced dopaminergic neurodegeneration, which corre

42 at GA has neuroprotective activity against 6-OHDA-induced oxidative stress via enhancement of cerebra

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

44 e protective effect of G-substrate against 6-OHDA.

45 greatly diminished neuroprotection against 6-OHDA.

46 the neuroprotective action of EGCG against 6-OHDA.

47 provide functional neuroprotection against 6-OHDA; therefore, targeted activation of the endogenous g

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

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

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

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

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

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

54 animal models, reserpinized rat model and 6-OHDA induced unilaterally lesioned rat model.

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

56 ral 6-OHDA treated group; and the sham and 6-OHDA treated groups underwent respective surgeries.

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

58 d into PD model animals, aphakia mice, and 6-OHDA-lesioned rats, mDA NPs differentiated into mDA neur

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

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

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

62 ll line MN9D showed that leptin attenuated 6-OHDA-induced apoptotic markers, including caspase-9 and

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

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

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

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

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

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

69 d153 was dramatically up-regulated by both 6-OHDA and MPP+.

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

71 he degeneration of dopaminergic neurons by 6-OHDA and may prove useful in the treatment of Parkinson

72 The H2O2 generated by 6-OHDA contributed toward the loss of anaerobic glycolysis

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

74 ve against depression of activity level by 6-OHDA than the non-recycling antioxidant, TEMPOL, in a mu

75 ated kinases (ERK1/2) activities caused by 6-OHDA toxicity.

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

77 ppears to underlie neuron death induced by 6-OHDA.

78 t does not further elevate death caused by 6-OHDA.

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 l

81 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, and

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

84 as essential for neuroprotection following 6-OHDA toxicity.

85 ng in Neuro-2a and SH-SY5Y cells following 6-OHDA treatment, and contributes to oxidopamine-mediated

86 ensity, and neuronal volume resulting from 6-OHDA lesion differed between regions, with the SNpc exhi

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

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

89 cathecolamine-producing SH-SY5Y cells from 6-OHDA-induced reactive oxygen species formation, caspase-

90 lated Akt and protected A9 DA neurons from 6-OHDA-induced toxicity.

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

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

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

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

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

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

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

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

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

100 The neurotoxin, 6-hydroxydopamine (6-OHDA) has been implicated in the neurodegenerative proce

101 ronal loss by injecting 6-hydroxydopamine (6-OHDA) in the dorsal GL or in the right substantia nigra

102 e containing or lacking 6-hydroxydopamine (6-OHDA) in the ipsilateral medial forebrain bundle (MFB).

103 that rats lesioned with 6-hydroxydopamine (6-OHDA) in the medial forebrain bundle display significant

104 atecholamine neurotoxin 6-hydroxydopamine (6-OHDA) induced a selective depletion of norepinephrine (b

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

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

107 nimals previously given 6-hydroxydopamine (6-OHDA) injections into the ascending DA pathways had grea

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

109 unilateral injection of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle, while sham surge

110 port that injections of 6-hydroxydopamine (6-OHDA) into the mouse striatum cause a local increase in

111 6-Hydroxydopamine (6-OHDA) is an oxidative neurotoxin used to injure catechol

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

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

114 gainst an intrastriatal 6-hydroxydopamine (6-OHDA) lesion in the common marmoset.

115 e-induced akinesia, rat 6-hydroxydopamine (6-OHDA) lesion model of drug-induced rotation, and MPTP-tr

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

117 nilateral intrastriatal 6-hydroxydopamine (6-OHDA) lesion model of PD on the number, morphology, and

118 xploited the unilateral 6-hydroxydopamine (6-OHDA) lesion model to assess the effect of minocycline o

119 nilateral nigrostriatal 6-hydroxydopamine (6-OHDA) lesion model using optogenetic and pharmacological

120 sy in mouse and the rat 6-hydroxydopamine (6-OHDA) lesion model.

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

122 ts following unilateral 6-hydroxydopamine (6-OHDA) lesion using an ultrafast opsin (Chronos).

123 ced rotations caused by 6-hydroxydopamine (6-OHDA) lesion.

124 ogression of a striatal 6-hydroxydopamine (6-OHDA) lesion.

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

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

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

128 Nigral 6-hydroxydopamine (6-OHDA) lesions or repeated D2-class antagonist injections

129 rodents with unilateral 6-hydroxydopamine (6-OHDA) lesions.

130 n a mouse intrastriatal 6-hydroxydopamine (6-OHDA) model of hemiparkinsonism.

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

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

133 evels in mice receiving 6-hydroxydopamine (6-OHDA) or rotenone to simulate PD.

134 eurodegeneration in the 6-hydroxydopamine (6-OHDA) PD model.

135 as neuroprotective in a 6-hydroxydopamine (6-OHDA) rat model of parkinsonism.

136 tor asymmetry in adult, 6-hydroxydopamine (6-OHDA) rats.

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

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

139 amine (DA) neurons from 6-hydroxydopamine (6-OHDA) toxicity.

140 ncreased in response to 6-hydroxydopamine (6-OHDA) treatment.

141 ilateral, intrastriatal 6-hydroxydopamine (6-OHDA) was used to investigate how dopamine depletion alt

142 en exposed to dopamine, 6-hydroxydopamine (6-OHDA), 4-hydroxy-2-nonenal (HNE), or H2O2, agents that a

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

144 6-Hydroxydopamine (6-OHDA), a PD mimetic, is widely used to model this neurod

145 shown that injection of 6-hydroxydopamine (6-OHDA), a toxin devoid of saporin, also damaged NTS catec

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

147 eatment with neurotoxin 6-hydroxydopamine (6-OHDA), leading to the biosynthesis of PGE2 and upregulat

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

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

150 ng systems arises after 6-hydroxydopamine (6-OHDA)-induced dopamine depletion, highlighting the centr

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

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

153 cently reported that in 6-hydroxydopamine (6-OHDA)-lesioned striatum, norepinephrine transporter (NET

154 rkably, after a partial 6-hydroxydopamine (6-OHDA)-mediated DA depletion ( approximately 70% in dorsa

155 n the hemi-Parkinsonian 6-hydroxydopamine (6-OHDA)-treated rat and 2) locomotion in the reserpine-tre

156 uced by the PD-mimetic, 6-hydroxydopamine (6-OHDA).

157 used ipsilaterally with 6-hydroxydopamine (6-OHDA).

158 he oxidative neurotoxin 6-hydroxydopamine (6-OHDA).

159 lly with the neurotoxin 6-hydroxydopamine (6-OHDA).

160 astriatal injections of 6-hydroxydopamine (6-OHDA).

161 minergic ROS generator, 6-hydroxydopamine (6-OHDA).

162 ain bundle injection of 6-hydroxydopamine (6-OHDA).

163 ative stress induced by 6-hydroxydopamine (6-OHDA).

164 noceptor antagonist) or 6-hydroxydopamine (6-OHDA, an agent that induces chemical sympathectomy) had

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

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

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

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

169 hysiological tonic, single-spike firing in 6-OHDA rats in vivo.

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

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

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

173 , which display a substantial reduction in 6-OHDA-induced neurotoxicity, as shown by increased surviv

174 ERK1/2 activation was confirmed in vivo in 6-OHDA-lesioned animals treated systemically with SKF38393

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

176 he survival factor Bcl-2 were decreased in 6-OHDA-treated cells, but message levels of genes lacking

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

178 lasma levels, or Cav1.3 LTCC deficiency in 6-OHDA-treated male mice.

179 BE(2)-M17 cells against toxins, including 6-OHDA and MG-132 (carbobenzoxy-L-leucyl- L-leucyl-L-leuci

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

181 PRX2 inhibited 6-OHDA-induced ASK1 activation by modulating the redox sta

182 ergic markers in response to intrastriatal 6-OHDA administration compared with wild-type (WT) litterm

183 ated degeneration induced by intrastriatal 6-OHDA in WT mice.

184 These findings indicate that intrastriatal 6-OHDA lesion differentially affects dopaminergic neurons

185 ther the effects of PAR-1 nor TPC on later 6-OHDA-induced behavioral deficits appeared to be mediated

186 with unilateral 6-hydroxydopamine lesions (6-OHDA) rendered dyskinetic with chronic L-DOPA treatment

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

188 In isolated mitochondria, 6-OHDA had negligible effects on complex I, inhibited comp

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

190 Neonatal 6-OHDA lesions actually give rise to a 5-HT axonal hyperin

191 n of direct pathway neurons after neonatal 6-OHDA lesions involves coupling of 5-HT2 receptors to the

192 The neurotoxin 6-OHDA was injected into the medial forebrain bundle (MFB)

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

194 Five or 21 d after nigral 6-OHDA injections or after 3, 7, or 21 d of D2 antagonist

195 Neither PRZ nor 6-OHDA affected the expression of cytokines, growth factor

196 rwent unilateral intrastriatal infusion of 6-OHDA (12.5mug).

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

198 Finally, co-oxidation of 6-OHDA by COX-2 triggered production of superoxide radical

199 The toxicity of 6-OHDA corresponds to the total collapse of anaerobic/aero

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

201 e associated with enhanced cytotoxicity of 6-OHDA in stably transfected PC12 cells.

202 e-reconstituted COX-2 induced oxidation of 6-OHDA in the course of its peroxidase (H(2)O(2)-dependent

203 ith cAMP several hours after initiation of 6-OHDA injury.

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

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

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

207 to elucidate the toxicological effects of 6-OHDA on energy metabolism in neuroblastoma (N-2A) cells.

208 O mice exhibit attenuated toxic effects of 6-OHDA on nigral dopaminergic cell counts, striatal dopami

209 radicals critical for both propagation of 6-OHDA oxidation and induction of oxidative stress in COX-

210 ssential for COX-2-dependent activation of 6-OHDA oxidation, oxygen radical production, oxidative str

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

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

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

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

215 minimal cytotoxicity, potent inhibition of 6-OHDA-induced mitochondrial membrane potential dissipatio

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

217 se of fully dopamine (DA)-depleted MSNs of 6-OHDA-treated mice, together with the beneficial effect o

218 protecting neuronal PC12 from toxicity of 6-OHDA.

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

220 cts of subthalamic nucleus (STN) lesion on 6-OHDA- or repeated D2 antagonist-induced changes in GP GA

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

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

223 antly, in vivo studies using MPTP, LPS, or 6-OHDA models revealed a greater attenuation of neuroinfla

224 ions (DL) fell more frequently than SAP or 6-OHDA rats.

225 t neuronal injuries induced by ischemia or 6-OHDA through the inhibition of apoptosis.

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

227 posure to SAP, targeted SAP conjugates, or 6-OHDA.

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

229 LRRK2 ultimately promoted 6-OHDA-induced cell death via positive modulation of HDAC3

230 as also observed in a mild progressive rat 6-OHDA-lesion model.

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

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

233 tive to controls in rats that had received 6-OHDA lesions and deposition of FG in the Acb core as com

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

235 However, selective 6-OHDA lesions of the dorsolateral striatum also had a pro

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

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

238 y, male Fischer 344 rats received striatal 6-OHDA lesions followed 1 week later by an intraventricula

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

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

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

242 The results showed that 6-OHDA significantly reduced the passive avoidance memory

243 inocycline treatment immediately after the 6-OHDA administration rescued neither TH(+) interneuron nu

244 The 6-OHDA incubation caused Nur77 translocation from the nucl

245 ions, and that NPC implantation before the 6-OHDA insult can create a host microenvironment conducive

246 It was found that the 6-OHDA lesion group failed to exhibit behavioral sensitiza

247 ed to the loss of motor control due to the 6-OHDA lesion.

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

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

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

251 , DNA damage, and neuroinflammation in the 6-OHDA rat model of PD, suggesting that SRY directly contr

252 The 6-OHDA treatments had no effect on horizontal activity or

253 The 6-OHDA treatments led to significant decreases in both pot

254 ificantly attenuated motor deficits in the 6-OHDA-hemilesioned rat model of PD.

255 d their projections to the striatum in the 6-OHDA-lesioned hemisphere.

256 to the dopamine-denervated striatum of the 6-OHDA-lesioned rat, sustained expression of each enzyme a

257 The 6-OHDA-lesioned rats that received repeated intravenous CD

258 The 6-OHDA-promoted cytotoxicity was largely blocked by TG4-15

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

260 Thus, 6-OHDA is capable of triggering multiple pathways associat

261 and sufficient for increased resistance to 6-OHDA in differentiated neuroblastoma cells, and that CRL

262 served in primary human neurons exposed to 6-OHDA or HNE.

263 astoma cells display higher sensitivity to 6-OHDA than differentiated cells.

264 sex differences in the brain's response to 6-OHDA, and imply that compensatory or neuroprotective mec

265 r PAR-1 and PAR-4 3 days before unilateral 6-OHDA administration (10 microg into the medial forebrain

266 t were rendered parkinsonian by unilateral 6-OHDA injection.

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

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

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

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

271 re rendered hemiparkinsonian by unilateral 6-OHDA lesions and primed with the D1R agonist SKF81297 (0

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

273 psilateral turning in rats with unilateral 6-OHDA nigrostriatal lesion and increased withdrawal laten

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

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

276 In unilaterally 6-OHDA-lesioned rats with LID, we show that the time cours

277 BMP7 pretreatment, as compared to vehicle/6-OHDA controls, had a significant reduction in methamphet

278 sessments of a rodent model of PD, wherein 6-OHDA was injected into the dorsolateral striatum of both

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

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

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

282 re euthanized 14 days after treatment with 6-OHDA and brains were stained with a tyrosine hydroxylase

283 itro studies with PC-12 cells treated with 6-OHDA and rotenone, respectively.

284 xperiment 2, rats were first injected with 6-OHDA and were then randomly assigned into one of the two

285 f TAAR1 KO mice unilaterally lesioned with 6-OHDA in the medial forebrain bundle resulted in more pro

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

287 A, compared with animals treated only with 6-OHDA into the nigrostriatal pathway.

288 imental conditions rats were injected with 6-OHDA into the right medial forebrain bundle.

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

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

291 neuronal cell lines (B65 and SH-SY5Y) with 6-OHDA resulted in repression of basal CRE transactivation

292 kinsonian mice (unilaterally lesioned with 6-OHDA) were treated daily for 3 weeks with a low dose of

293 rgic ventral midbrain neurons treated with 6-OHDA, 1-methyl-4-phenylpyridinium (MPP+), or alpha-synuc

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

295 2-fold (p < 0.05) in animals lesioned with 6-OHDA, compared with animals treated only with 6-OHDA int

296 that have been chemically denervated with 6-OHDA, suggesting that HED retention is a good surrogate

297 pathway MSNs after dopamine depletion with 6-OHDA.

298 XENP345/6-OHDA rats displayed attenuated amphetamine-induced rotat

299 models, reserpinized and 6-hydroxydopamine (OHDA)-induced unilateral lesioned rats.

300 kdown were adopted in the 6-hydroxydopamine (OHDA)-lesioned PC12 cells to investigate the mechanisms