ライフサイエンスコーパス: 6-hydroxydopamine

1 to a subsequent neurotoxic trigger (low-dose 6-hydroxydopamine).

2 rkinsonian rodent model induced by the toxin 6-hydroxydopamine.

3 ease based on neuronal PC12 cells exposed to 6-hydroxydopamine.

4 from death induced by hydrogen peroxide and 6-hydroxydopamine.

5 ons that antioxidants confer protection from 6-hydroxydopamine.

6 eeks after unilateral lesions of the SN with 6-hydroxydopamine.

7 eived unilateral intrastriatal injections of 6-hydroxydopamine.

8 lesioned as neonates (neonate lesioned) with 6-hydroxydopamine.

9 stress is compromised were more sensitive to 6-hydroxydopamine.

10 expression on neuronal PC12 cells exposed to 6-hydroxydopamine.

11 e neurons when administered 6 h prior to the 6-hydroxydopamine.

12 d 6 h later with an intranigral injection of 6-hydroxydopamine.

13 by intrastriatal injection of the neurotoxin 6-hydroxydopamine.

14 endoplasmic reticulum (ER) stress induced by 6-hydroxydopamine.

15 y following administration of the neurotoxin 6-hydroxydopamine.

16 when worms were exposed to the DA neurotoxin 6-hydroxydopamine.

17 triatal denervation in animals injected with 6-hydroxydopamine.

18 ceptibility of retinal dopaminergic cells to 6-hydroxydopamine.

19 ateral intrastriatal injections of the toxin 6-hydroxydopamine.

20 6-hydroxydopamine, 1-methyl-4-phenyl-pyridinium (MPP+),

21 ts treated with splanchnic ganglionectomy or 6-hydroxydopamine (6-OH-dopamine).

22 ative effects of the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) (unilateral intrastriatal inj

23 lateral lesion in substantia nigra (SN) with 6-hydroxydopamine (6-OHDA) affected differently the exci

24 ted by the Parkinsonism-inducing neurotoxins 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridini

25 naptic dopamine transporter (DAT), including 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridini

26 reated with the dopaminergic neuronal toxins 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridini

27 PD in vitro, including an oxidative stressor 6-hydroxydopamine (6-OHDA) and a proteasome inhibitor MG

28 has been investigated as a treatment in the 6-hydroxydopamine (6-OHDA) animal model of PD.

29 n's disease described in the pharmacological 6-hydroxydopamine (6-OHDA) animal models of Parkinson's

30 Rats lesioned with 6-hydroxydopamine (6-OHDA) as neonates exhibit behaviora

31 exacerbates vulnerability to the neurotoxin 6-hydroxydopamine (6-OHDA) both in vitro and in vivo.

32 activated at the transcriptional level in a 6-hydroxydopamine (6-OHDA) cellular model of PD.

33 neurotrophic factor GDNF in the unilaterally 6-hydroxydopamine (6-OHDA) denervated substantia nigra (

34 We previously found that 6-hydroxydopamine (6-OHDA) elicits sustained extracellul

35 The neurotoxin, 6-hydroxydopamine (6-OHDA) has been implicated in the ne

36 The neurotoxin 6-hydroxydopamine (6-OHDA) has been used extensively in

37 eroxide (TBHP) and of the dopaminergic toxin 6-hydroxydopamine (6-OHDA) in PC12 cells.

38 by 1-methyl-4-phenylpyridinium (MPP(+)) and 6-hydroxydopamine (6-OHDA) in primary DAergic neuron cul

39 we induce DAergic neuronal loss by injecting 6-hydroxydopamine (6-OHDA) in the dorsal GL or in the ri

40 sion of saline vehicle containing or lacking 6-hydroxydopamine (6-OHDA) in the ipsilateral medial for

41 tudy, we demonstrate that rats lesioned with 6-hydroxydopamine (6-OHDA) in the medial forebrain bundl

42 ministration of the catecholamine neurotoxin 6-hydroxydopamine (6-OHDA) induced a selective depletion

43 o investigate the in vivo effects of BMP7 on 6-hydroxydopamine (6-OHDA) induced lesioning of midbrain

44 Six weeks after 6-hydroxydopamine (6-OHDA) infusion into the medial fore

45 immunoreactive microglial profiles following 6-hydroxydopamine (6-OHDA) injection into ipsilateral st

46 Animals previously given 6-hydroxydopamine (6-OHDA) injections into the ascending

47 One week following two bilateral 6-hydroxydopamine (6-OHDA) injections into the mPFC, ani

48 aporin (SAP) into the basal forebrain and/or 6-hydroxydopamine (6-OHDA) into the caudate nucleus, res

49 Five rats received unilateral injection of 6-hydroxydopamine (6-OHDA) into the medial forebrain bun

50 D was induced with a unilateral injection of 6-hydroxydopamine (6-OHDA) into the medial forebrain bun

51 Here, we report that injections of 6-hydroxydopamine (6-OHDA) into the mouse striatum cause

52 triatal lesioning was performed by injecting 6-hydroxydopamine (6-OHDA) into the substantia nigra par

53 6-Hydroxydopamine (6-OHDA) is an oxidative neurotoxin us

54 While 6-hydroxydopamine (6-OHDA) is often used in animal model

55 The dopamine analogue 6-hydroxydopamine (6-OHDA) is selectively toxic to catec

56 6-Hydroxydopamine (6-OHDA) is widely used to selectively

57 igrostriatal dopamine system by injection of 6-hydroxydopamine (6-OHDA) lead to abnormal neuronal act

58 havioral protection against an intrastriatal 6-hydroxydopamine (6-OHDA) lesion in the common marmoset

59 use model of reserpine-induced akinesia, rat 6-hydroxydopamine (6-OHDA) lesion model of drug-induced

60 s of reserpine-induced akinesia, and the rat 6-hydroxydopamine (6-OHDA) lesion model of drug-induced

61 ffects of a partial unilateral intrastriatal 6-hydroxydopamine (6-OHDA) lesion model of PD on the num

62 We exploited the unilateral 6-hydroxydopamine (6-OHDA) lesion model to assess the ef

63 motor deficits in a unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) lesion model using optogeneti

64 neurons in the progressive Sauer and Oertel 6-hydroxydopamine (6-OHDA) lesion model, rats received p

65 ridol-induced catalepsy in mouse and the rat 6-hydroxydopamine (6-OHDA) lesion model.

66 44BNF(1)) hybrid rats following a unilateral 6-hydroxydopamine (6-OHDA) lesion of the nigrostriatal p

67 treating the symptoms of parkinsonism in the 6-hydroxydopamine (6-OHDA) lesion rat.

68 STN DBS in female rats following unilateral 6-hydroxydopamine (6-OHDA) lesion using an ultrafast ops

69 and amphetamine-induced rotations caused by 6-hydroxydopamine (6-OHDA) lesion.

70 n-1 (OP-1), on the progression of a striatal 6-hydroxydopamine (6-OHDA) lesion.

71 Administration of dopamine agonists to 6-hydroxydopamine (6-OHDA) lesioned rats enhances the ro

72 es from the striatum of intact or unilateral 6-hydroxydopamine (6-OHDA) lesioned rats of increasing a

73 n dopamine denervated striatum of unilateral 6-hydroxydopamine (6-OHDA) lesioned rats.

74 One model was 6-hydroxydopamine (6-OHDA) lesioning and the other was d

75 Rats were given unilateral 6-hydroxydopamine (6-OHDA) lesions and subsequently rece

76 N) on motor impairment induced by unilateral 6-hydroxydopamine (6-OHDA) lesions in the medial forebra

77 6-Hydroxydopamine (6-OHDA) lesions of brain noradrenergi

78 Rats with 6-hydroxydopamine (6-OHDA) lesions of the nigrostriatal

79 To this end, we tested animals with 6-hydroxydopamine (6-OHDA) lesions of the PL and IL mPFC

80 ced turning behavior in rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the SN.

81 phine administration in rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the substantia nig

82 Nigral 6-hydroxydopamine (6-OHDA) lesions or repeated D2-class

83 Partial 6-hydroxydopamine (6-OHDA) lesions were conducted in the

84 s not altered by decortication or unilateral 6-hydroxydopamine (6-OHDA) lesions.

85 striatal slices from rodents with unilateral 6-hydroxydopamine (6-OHDA) lesions.

86 tions were assessed in a mouse intrastriatal 6-hydroxydopamine (6-OHDA) model of hemiparkinsonism.

87 ioning (TPC) was found to be protective in a 6-hydroxydopamine (6-OHDA) model of the disease.

88 iatal catecholamine levels in the unilateral 6-hydroxydopamine (6-OHDA) mouse model of dopaminergic c

89 n the early neurochemical events involved in 6-hydroxydopamine (6-OHDA) neurotoxicity and the putativ

90 ive, central noradrenergic dennervation with 6-hydroxydopamine (6-OHDA) on the expression of type 4 p

91 ted with bilateral microinjections of either 6-hydroxydopamine (6-OHDA) or its vehicle into the NAcc

92 mine and metabolite levels in mice receiving 6-hydroxydopamine (6-OHDA) or rotenone to simulate PD.

93 s, into the area of neurodegeneration in the 6-hydroxydopamine (6-OHDA) PD model.

94 clic antidepressant was neuroprotective in a 6-hydroxydopamine (6-OHDA) rat model of parkinsonism.

95 of amelioration of motor asymmetry in adult, 6-hydroxydopamine (6-OHDA) rats.

96 cardiomyocyte growth was investigated using 6-hydroxydopamine (6-OHDA) to abolish early sympathetic

97 ortex (mPFC) were unilaterally lesioned with 6-hydroxydopamine (6-OHDA) to examine how dopamine (DA)

98 t study, we used the dopaminergic (DA) toxin 6-hydroxydopamine (6-OHDA) to model PD and explore the p

99 r (GDNF) protects dopamine (DA) neurons from 6-hydroxydopamine (6-OHDA) toxicity.

100 translocation were increased in response to 6-hydroxydopamine (6-OHDA) treatment.

101 The data indicate that the different 6-hydroxydopamine (6-OHDA) vulnerabilities of ventral me

102 e current studies, unilateral, intrastriatal 6-hydroxydopamine (6-OHDA) was used to investigate how d

103 h D3T for 24 h and then exposed to dopamine, 6-hydroxydopamine (6-OHDA), 4-hydroxy-2-nonenal (HNE), o

104 Neurotoxin lesions with 6-hydroxydopamine (6-OHDA), 5,7-dihydroxytryptamine (5,7

105 rn of neurodegeneration after treatment with 6-hydroxydopamine (6-OHDA), a neurotoxin commonly used t

106 tum 4 weeks after intrastriatal injection of 6-hydroxydopamine (6-OHDA), a neurotoxin selective for c

107 6-Hydroxydopamine (6-OHDA), a PD mimetic, is widely used

108 However, others have shown that injection of 6-hydroxydopamine (6-OHDA), a toxin devoid of saporin, a

109 tion of catechols, such as dopamine (DA) and 6-hydroxydopamine (6-OHDA), and resulting in oxidative s

110 phic factor (GDNF), when administered before 6-hydroxydopamine (6-OHDA), has been shown to prevent th

111 an SH-SY5Y - after treatment with neurotoxin 6-hydroxydopamine (6-OHDA), leading to the biosynthesis

112 nd neurotoxic lesions of DA neurons by using 6-hydroxydopamine (6-OHDA), to ascertain whether N/OFQ a

113 The neurotoxin 6-hydroxydopamine (6-OHDA), which is easily oxidized to

114 ed motor deficits and nigral DA cell loss in 6-hydroxydopamine (6-OHDA)-induced and rotenone-induced

115 The 6-hydroxydopamine (6-OHDA)-induced destruction of the ni

116 and indirect projecting systems arises after 6-hydroxydopamine (6-OHDA)-induced dopamine depletion, h

117 treadmill locomotion in rats with unilateral 6-hydroxydopamine (6-OHDA)-induced lesions of nigrostria

118 The effects of 6-hydroxydopamine (6-OHDA)-induced lesions of the dorsal

119 Severe 6-hydroxydopamine (6-OHDA)-induced neostriatal dopamine

120 mine receptors (D(2)DRs) in the unilaterally 6-hydroxydopamine (6-OHDA)-lesioned rat enhanced striata

121 ir ability to induce rotational behaviour in 6-hydroxydopamine (6-OHDA)-lesioned rats and to potentia

122 Prior studies in unilateral 6-hydroxydopamine (6-OHDA)-lesioned rats have primarily

123 orded in freely moving normal and unilateral 6-hydroxydopamine (6-OHDA)-lesioned rats using chronical

124 In unilateral 6-hydroxydopamine (6-OHDA)-lesioned rats, (+)-dinapsolin

125 We recently reported that in 6-hydroxydopamine (6-OHDA)-lesioned striatum, norepineph

126 Remarkably, after a partial 6-hydroxydopamine (6-OHDA)-mediated DA depletion ( appro

127 e-induced rotations in the hemi-Parkinsonian 6-hydroxydopamine (6-OHDA)-treated rat and 2) locomotion

128 were subsequently infused ipsilaterally with 6-hydroxydopamine (6-OHDA).

129 riatal injection of the oxidative neurotoxin 6-hydroxydopamine (6-OHDA).

130 ation induced chemically with the neurotoxin 6-hydroxydopamine (6-OHDA).

131 ors, followed by intrastriatal injections of 6-hydroxydopamine (6-OHDA).

132 city of the catecholaminergic ROS generator, 6-hydroxydopamine (6-OHDA).

133 lateral medial forebrain bundle injection of 6-hydroxydopamine (6-OHDA).

134 loying the parkinsonism-inducing neurotoxin, 6-hydroxydopamine (6-OHDA).

135 ter unilateral exposure to the DA neurotoxin 6-hydroxydopamine (6-OHDA).

136 rotein also potentiated the neurotoxicity of 6-hydroxydopamine (6-OHDA).

137 inergic pathway was unilaterally lesioned by 6-hydroxydopamine (6-OHDA).

138 amine neurons following in vivo lesions with 6-hydroxydopamine (6-OHDA).

139 d to an unilateral intrastriatal infusion of 6-hydroxydopamine (6-OHDA).

140 th resistance to oxidative stress induced by 6-hydroxydopamine (6-OHDA).

141 nuated cell death induced by the PD-mimetic, 6-hydroxydopamine (6-OHDA).

142 SNC following treatment with the neurotoxin 6-hydroxydopamine (6-OHDA); however, GFRalpha-1 expressi

143 (PRZ, an alpha-1 adrenoceptor antagonist) or 6-hydroxydopamine (6-OHDA, an agent that induces chemica

144 l ganglia of rats, lesioned as neonates with 6-hydroxydopamine (6-OHDA, intracisternally) on the thir

145 cit and cerebral oxidative stress induced by 6-hydroxydopamine (6-OHDA; 8 mug/2 muL) injected into th

146 eral intracerebroventricular injections with 6-hydroxydopamine (6-OHDA; a model of Lesch-Nyhan syndro

147 located in the SNR, which were resistant to (6-hydroxydopamine) 6-OHDA, was established by their expr

148 clinical lesions of the striatum with either 6-hydroxydopamine (6OHDA) or quinolinic acid (QA) exagge

149 or chemical sympathectomy of the spleen with 6-hydroxydopamine (6OHDA; -14d) exacerbated injury after

150 6-Hydroxydopamine administration resulted in an increase

151 In addition, Fyn-depleted mice lesioned with 6-hydroxydopamine also failed to exhibit l-DOPA-induced

152 tomy eliminated both the survival benefit of 6-hydroxydopamine and monocyte recruitment, suggesting t

153 were given a unilateral dopamine lesion with 6-hydroxydopamine and primed with a chronic regimen of l

154 ts of unilateral nigrostriatal ablation with 6-hydroxydopamine and subsequent treatment with levodopa

155 fluorescent protein) mice were lesioned with 6-hydroxydopamine and subsequently treated with L-DOPA t

156 s induced by the intra-striatal injection of 6-hydroxydopamine, and mice were treated with either sal

157 dult mice by the intra-striatal injection of 6-hydroxydopamine, and PD mice were treated with 1mg/kg

158 ncreased in the presence of ascorbic acid or 6-hydroxydopamine as pro-oxidants.

159 ptors in explant culture with the neurotoxin 6-hydroxydopamine at early stages of gland development r

160 nt (scid) mouse that was depleted of NE with 6-hydroxydopamine before reconstitution with a clone of

161 rm of Nix, protects neuronal PC12 cells from 6-hydroxydopamine but not from nerve growth factor depri

162 ress created by neurotoxins such as MPTP and 6-hydroxydopamine can upregulate VGluT2 in surviving DA

163 how that dopamine depletion in adult rats by 6-hydroxydopamine caused a significant decrease in stria

164 vivo on the effects of L-dopa in the 6OHDA (6-hydroxydopamine) contralateral turning model.

165 inistration of the noradrenergic neurotoxin, 6-hydroxydopamine, did not block the effect of IL-1beta.

166 r adult rats were unilaterally lesioned with 6-hydroxydopamine, fast-scan cyclic voltammetry at Nafio

167 nigrostriatal dopamine system ablation with 6-hydroxydopamine followed by twice-daily treatment with

168 encephalon at 3, 7, 10, 14 and 21 days after 6-hydroxydopamine had been injected into the medial fore

169 synergistic attenuation of motor deficits in 6-hydroxydopamine hemilesioned rats and 1-methyl-4-pheny

170 mg/Kg) attenuated dyskinesias expression in 6-hydroxydopamine hemilesioned rats primed with L-DOPA,

171 nimals received an injection of 25 microg of 6-hydroxydopamine hydrobromide (6-OHDA) midway between t

172 halamus were lesioned by i.c.v. injection of 6-hydroxydopamine immediately prior to the induction of

173 atal dopamine neurons against the effects of 6-hydroxydopamine in aged as well as young adult rats.

174 ctive destruction of dopamine terminals with 6-hydroxydopamine, indicating that GABA release originat

175 onal cells protects against staurosporin and 6-hydroxydopamine induced apoptosis and cell death.

176 e mitochondrial JNK plays in the etiology of 6-hydroxydopamine-induced (6-OHDA) oxidative stress, mit

177 We found that meclizine protected against 6-hydroxydopamine-induced apoptosis and cell death in bo

178 These cells are vulnerable to hypoxia- and 6-hydroxydopamine-induced cell death, respectively.

179 rat nigrostriatal dopaminergic pathway from 6-hydroxydopamine-induced damage.

180 re neuronal activity in the STN of rats with 6-hydroxydopamine-induced lesions of the nigrostriatal p

181 factor (GDNF) can completely protect against 6-hydroxydopamine-induced loss of nigral dopamine neuron

182 l death, neurotoxin-induced neuronal injury, 6-hydroxydopamine-induced Parkinson's dopaminergic neuro

183 GDNF pretreatment also protected against 6-hydroxydopamine-induced reductions in striatal DOPAC l

184 ventral striatal dopaminergic terminals with 6-hydroxydopamine infusions into the nucleus accumbens d

185 Depletion of dopamine by 6-hydroxydopamine injection on postnatal day 4 did not a

186 cells into rats rendered hemiparkinsonian by 6-hydroxydopamine injection.

187 tal dopamine depletions, rats first received 6-hydroxydopamine injections into the nigrostriatal bund

188 tive lesion of A5 cells by microinjection of 6-hydroxydopamine into the pons showed no deficits to st

189 Injections of 6-hydroxydopamine into the vPAG, which killed 55-65% of

190 Following a unilateral 6-hydroxydopamine lesion A, A(A) and double A-A(A) knock

191 The 6-hydroxydopamine lesion affected B(max) (control, 402 +

192 otection of SN neurons following progressive 6-hydroxydopamine lesion and was associated with decreas

193 Likewise, 6-hydroxydopamine lesion did not impact GABA or glutamat

194 motor neglect after unilateral nigrostriatal 6-hydroxydopamine lesion in mice.

195 rat model of Parkinson's disease, unilateral 6-hydroxydopamine lesion in the substantia nigra, [3H]AA

196 6-Hydroxydopamine lesion led to parkinsonian motor impai

197 ts in the motor cortex of chronic unilateral 6-hydroxydopamine lesion male rats performing a skilled

198 Using the 6-hydroxydopamine lesion model of Parkinson's disease an

199 The present study used the rat unilateral 6-hydroxydopamine lesion model of Parkinson's disease to

200 n of NMDA receptor subunits (NRs) in the rat 6-hydroxydopamine lesion model of parkinsonism.

201 f STN inputs to PV(+) neurons in the chronic 6-hydroxydopamine lesion model of PD.

202 ects of the GDNF product in an intrastriatal 6-hydroxydopamine lesion model.

203 ue-Dawley rats initially received unilateral 6-hydroxydopamine lesion of the medial forebrain bundle.

204 Furthermore, a unilateral 6-hydroxydopamine lesion of the mesostriatal dopamine sy

205 n of the adult rat by using a combination of 6-hydroxydopamine lesion of the substantia nigra dopamin

206 ects against nigrostriatal tract loss in the 6-hydroxydopamine lesion rat model of Parkinson's diseas

207 Bilateral 6-hydroxydopamine lesion reduced long-term but not short

208 otational behavior in rats with a unilateral 6-hydroxydopamine lesion was used as an index of psychom

209 Neonatal rat 6-hydroxydopamine lesion-induced hyperactivity was used

210 walking states, before and after unilateral 6-hydroxydopamine lesion.

211 ctances, and their responsiveness to chronic 6-hydroxydopamine lesion.

212 In addition, 6-hydroxydopamine lesioned mice showed extended survival

213 In addition, in a rat 6-hydroxydopamine lesioned model of PD, chronic levodopa

214 When transplanted into the 6-hydroxydopamine lesioned Parkinsonian rats, these cogr

215 basal ganglia were studied in the unilateral 6-hydroxydopamine lesioned rat model of PD.

216 l spiking activity in control and unilateral 6-hydroxydopamine lesioned rats performing a skilled for

217 n and ipsilateral striatal Fos expression in 6-hydroxydopamine lesioned rats.

218 d the activity of L-DOPA in the unilaterally 6-hydroxydopamine-lesioned (6-OHDA) rat, a model of Park

219 ional behavior induced by apomorphine in the 6-hydroxydopamine-lesioned animal models of Parkinson's

220 Sham- and 6-hydroxydopamine-lesioned mice were subjected to the no

221 ed transcriptome analyses in the striatum in 6-hydroxydopamine-lesioned mice.

222 When transplanted into the neostriata of 6-hydroxydopamine-lesioned parkinsonian rats, the dopami

223 Toxin-based models, such as the 6-hydroxydopamine-lesioned rat and 1-methyl-4-phenyl-1,2

224 omorphine-induced rotational behavior in the 6-hydroxydopamine-lesioned rat model of hemiparkinsonism

225 omorphine-induced rotational behavior in the 6-hydroxydopamine-lesioned rat model of hemiparkinsonism

226 In the 6-hydroxydopamine-lesioned rat model, this compound was

227 Preliminary examination in the unilateral 6-hydroxydopamine-lesioned rat revealed a modest but sig

228 A in a rat model of Parkinson's disease (the 6-hydroxydopamine-lesioned rat), dosed at 30 mg/kg orall

229 oth potentiated the effects of L-DOPA in the 6-hydroxydopamine-lesioned rat, a model of Parkinson's d

230 e neuroblastoma (NBP2) cells into striata of 6-hydroxydopamine-lesioned rats (an animal model of PD)

231 Seven unilaterally 6-hydroxydopamine-lesioned rats (dopaminergic denervatio

232 sion were compared in the STN of control and 6-hydroxydopamine-lesioned rats and mice.

233 nificantly increased in ON L-DOPA dyskinetic 6-hydroxydopamine-lesioned rats, suggesting that increas

234 nduced dopamine-depleted mice and in chronic 6-hydroxydopamine-lesioned rats.

235 of l-dopa-induced contralateral rotations in 6-hydroxydopamine-lesioned rats.

236 ions can release dopamine in the midbrain of 6-hydroxydopamine-lesioned rats.

237 , IGF-I, and bFGF and then transplanted into 6-hydroxydopamine-lesioned rats.

238 ent inhibition of locomotor hyperactivity in 6-hydroxydopamine-lesioned rats.

239 ame-day lesion-transplant paradigm) into the 6-hydroxydopamine-lesioned striatum of rats significantl

240 porcine ventral mesencephalic tissue in the 6-hydroxydopamine-lesioned, nonimmunosuppressed rat indu

241 l KOs and caffeine-pretreated mice following 6-hydroxydopamine lesioning.

242 Analysis of LTP in animals with unilateral 6-hydroxydopamine lesions (6-OHDA) rendered dyskinetic w

243 ias were evaluated twice a week in mice with 6-hydroxydopamine lesions during long-term L-DOPA (25 mg

244 t, neurons recorded in rats with ipsilateral 6-hydroxydopamine lesions failed to show attentional sig

245 We made localized intrastriatal 6-hydroxydopamine lesions in rats and recorded within th

246 6-hydroxydopamine lesions of the A5-7 groups or ibotenic

247 the present study, we examined the effect of 6-hydroxydopamine lesions of the medial prefrontal corte

248 munocytochemistry in animals with unilateral 6-hydroxydopamine lesions of the nigrostriatal bundle.

249 ed DAMGO-induced motor activity that follows 6-hydroxydopamine lesions of the nucleus accumbens.

250 arm use, in contrast to rats with unilateral 6-hydroxydopamine lesions of the substantia nigra.

251 al caudate-putamen were determined following 6-hydroxydopamine lesions of the ventral tegmental area

252 taneous object recognition to test rats with 6-hydroxydopamine lesions targeted at the core or medial

253 found that the acute hypertension induced by 6-hydroxydopamine lesions was immediately reversed and t

254 denervated striatum of rats with unilateral 6-hydroxydopamine lesions.

255 Here, we show that 6-hydroxydopamine-mediated ablation of the mouse periphe

256 Using a model of 6-hydroxydopamine-mediated noradrenergic nerve ablation,

257 lective dopamine (DA) depleting lesions with 6-hydroxydopamine microinjection into the SN, CPu, and N

258 ydroxy-N,N-di-n-propyl-2-aminotetralin) in a 6-hydroxydopamine model of Parkinson's disease.

259 n the dopamine-depleted striatum of a rodent 6-hydroxydopamine model of Parkinson's disease.

260 e response to achieve neuroprotection in the 6-hydroxydopamine model.

261 ed a stereotaxic injection of 8 mug/2 muL of 6-hydroxydopamine (n = 6) or saline solution (n = 4) in

262 halic dopaminergic neurons protected against 6-hydroxydopamine neurotoxicity by suppressing apoptosis

263 ty in two PD animal models, reserpinized and 6-hydroxydopamine (OHDA)-induced unilateral lesioned rat

264 r77, and Nur77 knockdown were adopted in the 6-hydroxydopamine (OHDA)-lesioned PC12 cells to investig

265 ctivity in basolateral amygdala in rats with 6-hydroxydopamine or sham lesions of the ipsilateral mid

266 tures of Sprague-Dawley rats with unilateral 6-hydroxydopamine or sham lesions of the rostral accumbe

267 We microinjected 6-hydroxydopamine or vitamin C into nucleus tractus soli

268 al models of PD induced by either oxidative (6-hydroxydopamine) or mitochondrial (N-methyl-4-phenyl-1

269 were destroyed via intraocular injection of 6-hydroxydopamine over 2 successive days.

270 d quantification of DAT in rodents using the 6-hydroxydopamine Parkinson disease rat model.

271 used microPET to study unilaterally lesioned 6-hydroxydopamine rats that developed levodopa-induced a

272 t AIM severity, following induction of AIMs, 6-hydroxydopamine rats were injected with Daun02 in the

273 uction in SN of both unprimed and dyskinetic 6-hydroxydopamine rats, consistent with opposite adaptiv

274 Rats unilaterally lesioned with 6-hydroxydopamine received transplants that were incubat

275 hway produced in rats following injection of 6-hydroxydopamine result in a neurochemical profile simi

276 Intrastriatal injection of 6-hydroxydopamine results in selective toxicity to these

277 ation of the PF in the rat and determined if 6-hydroxydopamine SN lesions cause PF neuron degeneratio

278 n cerebellar granule neurons by glutamate or 6-hydroxydopamine stimulation but not potassium withdraw

279 , a group of animals received a high dose of 6-hydroxydopamine that normally would yield a severe los

280 Rats were administered 6-hydroxydopamine to induce brainstem lesions, causing a

281 s disease, including unilateral infusions of 6-hydroxydopamine to the medial forebrain bundle and per

282 Using two PD models, the traditional 6-hydroxydopamine toxic lesion and a genetic model with

283 peroxide dismutase showed no protection from 6-hydroxydopamine toxicity in either brain region.

284 racellular or nonmitochondrial mechanisms in 6-hydroxydopamine toxicity, the compartmentalization of

285 le for mitochondrially derived superoxide in 6-hydroxydopamine toxicity.

286 ase (PD) has primarily been performed in the 6-hydroxydopamine toxin model.

287 in the dyskinetic animals compared with the 6-hydroxydopamine-treated and control rats.

288 corded from the basal ganglia of control and 6-hydroxydopamine-treated hemi-parkinsonian rats anesthe

289 mal models of DA neuron loss and PD, such as 6-hydroxydopamine-treated mice or rats and 1-methyl-4-ph

290 lantation of these cells into the striata of 6-hydroxydopamine-treated rats at the neuronal progenito

291 to potassium removal, glutamate toxicity, or 6-hydroxydopamine treatment and found that clone 17a tra

292 ulture and prevents their degeneration after 6-hydroxydopamine treatment in vivo.

293 t was ablated by chemical sympathectomy with 6-hydroxydopamine treatment.

294 First, rats were exposed to a mild dose of 6-hydroxydopamine unilaterally into the nigrostriatal do

295 xperiment 1, rats received microinfusions of 6-hydroxydopamine unilaterally to induce dopamine termin

296 esion produced by intrastriatal injection of 6-hydroxydopamine was indistinguishable between WT and A

297 rplexiform cells (DA-IPCs) were destroyed by 6-hydroxydopamine was measured behaviorally.

298 In the present study, 6-hydroxydopamine was used to lesion the dorsal striatum

299 6-Hydroxydopamine was used to produce a model of Parkins

300 athway had been eliminated unilaterally with 6-hydroxydopamine, we injected a Cre-dependent virus cod