ライフサイエンスコーパス: hydroxydopamine

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

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

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

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

5 s that antioxidants confer protection from 6-hydroxydopamine.

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

7 ved unilateral intrastriatal injections of 6-hydroxydopamine.

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

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

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

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

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

13 doplasmic reticulum (ER) stress induced by 6-hydroxydopamine.

14 intrastriatal injection of the neurotoxin 6-hydroxydopamine.

15 following administration of the neurotoxin 6-hydroxydopamine.

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

17 iatal denervation in animals injected with 6-hydroxydopamine.

18 ptibility of retinal dopaminergic cells to 6-hydroxydopamine.

19 eral intrastriatal injections of the toxin 6-hydroxydopamine.

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

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

22 ive effects of the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) (unilateral intrastriatal injec

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

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

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

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

27 in vitro, including an oxidative stressor 6-hydroxydopamine (6-OHDA) and a proteasome inhibitor MG-1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 ive degeneration induced by the neurotoxin 6-hydroxydopamine (6-OHDA) injected into the striatum.

46 munoreactive microglial profiles following 6-hydroxydopamine (6-OHDA) injection into ipsilateral stri

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

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

49 orin (SAP) into the basal forebrain and/or 6-hydroxydopamine (6-OHDA) into the caudate nucleus, respe

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

51 was induced with a unilateral injection of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundl

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

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

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

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

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

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

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

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

60 e model of reserpine-induced akinesia, rat 6-hydroxydopamine (6-OHDA) lesion model of drug-induced ro

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

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

63 tor deficits in a unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) lesion model using optogenetic

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

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

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

67 nd amphetamine-induced rotations caused by 6-hydroxydopamine (6-OHDA) lesion.

68 1 (OP-1), on the progression of a striatal 6-hydroxydopamine (6-OHDA) lesion.

69 Administration of dopamine agonists to 6-hydroxydopamine (6-OHDA) lesioned rats enhances the rota

70 from the striatum of intact or unilateral 6-hydroxydopamine (6-OHDA) lesioned rats of increasing age

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

72 One model was 6-hydroxydopamine (6-OHDA) lesioning and the other was dir

73 Rats were given unilateral 6-hydroxydopamine (6-OHDA) lesions and subsequently receiv

74 on motor impairment induced by unilateral 6-hydroxydopamine (6-OHDA) lesions in the medial forebrain

75 6-Hydroxydopamine (6-OHDA) lesions of brain noradrenergic

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

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

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

79 ine administration in rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the substantia nigra

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

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

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

83 riatal slices from rodents with unilateral 6-hydroxydopamine (6-OHDA) lesions.

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

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

86 tal catecholamine levels in the unilateral 6-hydroxydopamine (6-OHDA) mouse model of dopaminergic cel

87 the early neurochemical events involved in 6-hydroxydopamine (6-OHDA) neurotoxicity and the putative

88 e, central noradrenergic dennervation with 6-hydroxydopamine (6-OHDA) on the expression of type 4 pho

89 d with bilateral microinjections of either 6-hydroxydopamine (6-OHDA) or its vehicle into the NAcc an

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

91 into the area of neurodegeneration in the 6-hydroxydopamine (6-OHDA) PD model.

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

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

94 ardiomyocyte growth was investigated using 6-hydroxydopamine (6-OHDA) to abolish early sympathetic in

95 tex (mPFC) were unilaterally lesioned with 6-hydroxydopamine (6-OHDA) to examine how dopamine (DA) as

96 study, we used the dopaminergic (DA) toxin 6-hydroxydopamine (6-OHDA) to model PD and explore the pro

97 3,6-tetrahydropyridine toxicity in mice or 6-hydroxydopamine (6-OHDA) toxicity in rats.

98 protects midbrain dopamine neurons against 6-hydroxydopamine (6-OHDA) toxicity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 The 6-hydroxydopamine (6-OHDA)-induced destruction of the nigr

115 d indirect projecting systems arises after 6-hydroxydopamine (6-OHDA)-induced dopamine depletion, hig

116 eadmill locomotion in rats with unilateral 6-hydroxydopamine (6-OHDA)-induced lesions of nigrostriata

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

118 Severe 6-hydroxydopamine (6-OHDA)-induced neostriatal dopamine (D

119 ne receptors (D(2)DRs) in the unilaterally 6-hydroxydopamine (6-OHDA)-lesioned rat enhanced striatal

120 ability to induce rotational behaviour in 6-hydroxydopamine (6-OHDA)-lesioned rats and to potentiate

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

122 ded in freely moving normal and unilateral 6-hydroxydopamine (6-OHDA)-lesioned rats using chronically

123 In unilateral 6-hydroxydopamine (6-OHDA)-lesioned rats, (+)-dinapsoline

124 We recently reported that in 6-hydroxydopamine (6-OHDA)-lesioned striatum, norepinephri

125 Remarkably, after a partial 6-hydroxydopamine (6-OHDA)-mediated DA depletion ( approxi

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

127 re subsequently infused ipsilaterally with 6-hydroxydopamine (6-OHDA).

128 atal injection of the oxidative neurotoxin 6-hydroxydopamine (6-OHDA).

129 ion induced chemically with the neurotoxin 6-hydroxydopamine (6-OHDA).

130 s, followed by intrastriatal injections of 6-hydroxydopamine (6-OHDA).

131 ty of the catecholaminergic ROS generator, 6-hydroxydopamine (6-OHDA).

132 teral medial forebrain bundle injection of 6-hydroxydopamine (6-OHDA).

133 ying the parkinsonism-inducing neurotoxin, 6-hydroxydopamine (6-OHDA).

134 r unilateral exposure to the DA neurotoxin 6-hydroxydopamine (6-OHDA).

135 tein also potentiated the neurotoxicity of 6-hydroxydopamine (6-OHDA).

136 ergic pathway was unilaterally lesioned by 6-hydroxydopamine (6-OHDA).

137 ine neurons following in vivo lesions with 6-hydroxydopamine (6-OHDA).

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

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

140 ated cell death induced by the PD-mimetic, 6-hydroxydopamine (6-OHDA).

141 NC following treatment with the neurotoxin 6-hydroxydopamine (6-OHDA); however, GFRalpha-1 expression

142 RZ, an alpha-1 adrenoceptor antagonist) or 6-hydroxydopamine (6-OHDA, an agent that induces chemical

143 ganglia of rats, lesioned as neonates with 6-hydroxydopamine (6-OHDA, intracisternally) on the third

144 t and cerebral oxidative stress induced by 6-hydroxydopamine (6-OHDA; 8 mug/2 muL) injected into the

145 al intracerebroventricular injections with 6-hydroxydopamine (6-OHDA; a model of Lesch-Nyhan syndrome

146 cated in the SNR, which were resistant to (6-hydroxydopamine) 6-OHDA, was established by their expres

147 inical lesions of the striatum with either 6-hydroxydopamine (6OHDA) or quinolinic acid (QA) exaggera

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

149 6-Hydroxydopamine administration resulted in an increase i

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

151 my eliminated both the survival benefit of 6-hydroxydopamine and monocyte recruitment, suggesting tha

152 re given a unilateral dopamine lesion with 6-hydroxydopamine and primed with a chronic regimen of l-D

153 of unilateral nigrostriatal ablation with 6-hydroxydopamine and subsequent treatment with levodopa,

154 uorescent protein) mice were lesioned with 6-hydroxydopamine and subsequently treated with L-DOPA to

155 induced by the intra-striatal injection of 6-hydroxydopamine, and mice were treated with either salin

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

157 reased in the presence of ascorbic acid or 6-hydroxydopamine as pro-oxidants.

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

159 of Nix, protects neuronal PC12 cells from 6-hydroxydopamine but not from nerve growth factor depriva

160 w that dopamine depletion in adult rats by 6-hydroxydopamine caused a significant decrease in striata

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

162 6-Hydroxydopamine decreased tissue concentrations of dopam

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

164 adult rats were unilaterally lesioned with 6-hydroxydopamine, fast-scan cyclic voltammetry at Nafion-

165 igrostriatal dopamine system ablation with 6-hydroxydopamine followed by twice-daily treatment with l

166 cephalon at 3, 7, 10, 14 and 21 days after 6-hydroxydopamine had been injected into the medial forebr

167 nergistic attenuation of motor deficits in 6-hydroxydopamine hemilesioned rats and 1-methyl-4-phenyl-

168 g/Kg) attenuated dyskinesias expression in 6-hydroxydopamine hemilesioned rats primed with L-DOPA, wi

169 mals received an injection of 25 microg of 6-hydroxydopamine hydrobromide (6-OHDA) midway between the

170 lamus were lesioned by i.c.v. injection of 6-hydroxydopamine immediately prior to the induction of mo

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

172 ive destruction of dopamine terminals with 6-hydroxydopamine, indicating that GABA release originated

173 al cells protects against staurosporin and 6-hydroxydopamine induced apoptosis and cell death.

174 mitochondrial JNK plays in the etiology of 6-hydroxydopamine-induced (6-OHDA) oxidative stress, mitoc

175 We found that meclizine protected against 6-hydroxydopamine-induced apoptosis and cell death in both

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

177 at nigrostriatal dopaminergic pathway from 6-hydroxydopamine-induced damage.

178 eliorated behavioral deficits in rats with 6-hydroxydopamine-induced hemiparkinsonism.

179 neuronal activity in the STN of rats with 6-hydroxydopamine-induced lesions of the nigrostriatal pat

180 ctor (GDNF) can completely protect against 6-hydroxydopamine-induced loss of nigral dopamine neurons

181 death, neurotoxin-induced neuronal injury, 6-hydroxydopamine-induced Parkinson's dopaminergic neurona

182 GDNF pretreatment also protected against 6-hydroxydopamine-induced reductions in striatal DOPAC lev

183 ntral striatal dopaminergic terminals with 6-hydroxydopamine infusions into the nucleus accumbens did

184 Depletion of dopamine by 6-hydroxydopamine injection on postnatal day 4 did not aff

185 lls into rats rendered hemiparkinsonian by 6-hydroxydopamine injection.

186 l dopamine depletions, rats first received 6-hydroxydopamine injections into the nigrostriatal bundle

187 Injections of 6-hydroxydopamine into the brainstem did not reduce the de

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

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

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

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

192 ection of SN neurons following progressive 6-hydroxydopamine lesion and was associated with decreased

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

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

195 t model of Parkinson's disease, unilateral 6-hydroxydopamine lesion in the substantia nigra, [3H]AA a

196 6-Hydroxydopamine lesion led to parkinsonian motor impairm

197 Using the 6-hydroxydopamine lesion model of Parkinson's disease and

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

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

200 ts of the GDNF product in an intrastriatal 6-hydroxydopamine lesion model.

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

202 Furthermore, a unilateral 6-hydroxydopamine lesion of the mesostriatal dopamine syst

203 of the adult rat by using a combination of 6-hydroxydopamine lesion of the substantia nigra dopaminer

204 Bilateral 6-hydroxydopamine lesion reduced long-term but not short-t

205 ational behavior in rats with a unilateral 6-hydroxydopamine lesion was used as an index of psychomot

206 Neonatal rat 6-hydroxydopamine lesion-induced hyperactivity was used as

207 alking states, before and after unilateral 6-hydroxydopamine lesion.

208 cumbens and caudate-putamen, 4 weeks after 6-hydroxydopamine lesion.

209 ances, and their responsiveness to chronic 6-hydroxydopamine lesion.

210 In addition, 6-hydroxydopamine lesioned mice showed extended survival a

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

212 When transplanted into the 6-hydroxydopamine lesioned Parkinsonian rats, these cograf

213 sal ganglia were studied in the unilateral 6-hydroxydopamine lesioned rat model of PD.

214 spiking activity in control and unilateral 6-hydroxydopamine lesioned rats performing a skilled forel

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

216 the activity of L-DOPA in the unilaterally 6-hydroxydopamine-lesioned (6-OHDA) rat, a model of Parkin

217 In the 6-hydroxydopamine-lesioned animal model of Parkinson's dis

218 nal behavior induced by apomorphine in the 6-hydroxydopamine-lesioned animal models of Parkinson's di

219 Sham- and 6-hydroxydopamine-lesioned mice were subjected to the nove

220 transcriptome analyses in the striatum in 6-hydroxydopamine-lesioned mice.

221 When transplanted into the neostriata of 6-hydroxydopamine-lesioned parkinsonian rats, the dopamine

222 Toxin-based models, such as the 6-hydroxydopamine-lesioned rat and 1-methyl-4-phenyl-1,2,3

223 orphine-induced rotational behavior in the 6-hydroxydopamine-lesioned rat model of hemiparkinsonism a

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

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

226 in a rat model of Parkinson's disease (the 6-hydroxydopamine-lesioned rat), dosed at 30 mg/kg orally.

227 h potentiated the effects of L-DOPA in the 6-hydroxydopamine-lesioned rat, a model of Parkinson's dis

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

229 Seven unilaterally 6-hydroxydopamine-lesioned rats (dopaminergic denervation

230 on were compared in the STN of control and 6-hydroxydopamine-lesioned rats and mice.

231 ficantly increased in ON L-DOPA dyskinetic 6-hydroxydopamine-lesioned rats, suggesting that increased

232 ns can release dopamine in the midbrain of 6-hydroxydopamine-lesioned rats.

233 uced dopamine-depleted mice and in chronic 6-hydroxydopamine-lesioned rats.

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

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

236 t inhibition of locomotor hyperactivity in 6-hydroxydopamine-lesioned rats.

237 e-day lesion-transplant paradigm) into the 6-hydroxydopamine-lesioned striatum of rats significantly

238 orcine ventral mesencephalic tissue in the 6-hydroxydopamine-lesioned, nonimmunosuppressed rat induce

239 KOs and caffeine-pretreated mice following 6-hydroxydopamine lesioning.

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

241 s were evaluated twice a week in mice with 6-hydroxydopamine lesions during long-term L-DOPA (25 mg/k

242 neurons recorded in rats with ipsilateral 6-hydroxydopamine lesions failed to show attentional signa

243 We made localized intrastriatal 6-hydroxydopamine lesions in rats and recorded within the

244 6-hydroxydopamine lesions of the A5-7 groups or ibotenic a

245 e present study, we examined the effect of 6-hydroxydopamine lesions of the medial prefrontal cortex

246 nocytochemistry in animals with unilateral 6-hydroxydopamine lesions of the nigrostriatal bundle.

247 Unilateral 6-hydroxydopamine lesions of the nigrostriatal system were

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

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

250 caudate-putamen were determined following 6-hydroxydopamine lesions of the ventral tegmental area an

251 neous object recognition to test rats with 6-hydroxydopamine lesions targeted at the core or medial s

252 und that the acute hypertension induced by 6-hydroxydopamine lesions was immediately reversed and the

253 enervated striatum of rats with unilateral 6-hydroxydopamine lesions.

254 Here, we show that 6-hydroxydopamine-mediated ablation of the mouse periphera

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

256 ctive dopamine (DA) depleting lesions with 6-hydroxydopamine microinjection into the SN, CPu, and NAS

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

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

259 response to achieve neuroprotection in the 6-hydroxydopamine model.

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

261 lic dopaminergic neurons protected against 6-hydroxydopamine neurotoxicity by suppressing apoptosis t

262 in two PD animal models, reserpinized and 6-hydroxydopamine (OHDA)-induced unilateral lesioned rats.

263 7, and Nur77 knockdown were adopted in the 6-hydroxydopamine (OHDA)-lesioned PC12 cells to investigat

264 ivity in basolateral amygdala in rats with 6-hydroxydopamine or sham lesions of the ipsilateral midbr

265 res of Sprague-Dawley rats with unilateral 6-hydroxydopamine or sham lesions of the rostral accumbens

266 We microinjected 6-hydroxydopamine or vitamin C into nucleus tractus solita

267 models of PD induced by either oxidative (6-hydroxydopamine) or mitochondrial (N-methyl-4-phenyl-1,2

268 ere destroyed via intraocular injection of 6-hydroxydopamine over 2 successive days.

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

270 ed microPET to study unilaterally lesioned 6-hydroxydopamine rats that developed levodopa-induced abn

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

272 tion in SN of both unprimed and dyskinetic 6-hydroxydopamine rats, consistent with opposite adaptive

273 Rats unilaterally lesioned with 6-hydroxydopamine received transplants that were incubated

274 ay produced in rats following injection of 6-hydroxydopamine result in a neurochemical profile simila

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

276 ion of the PF in the rat and determined if 6-hydroxydopamine SN lesions cause PF neuron degeneration.

277 cerebellar granule neurons by glutamate or 6-hydroxydopamine stimulation but not potassium withdrawal

278 a group of animals received a high dose of 6-hydroxydopamine that normally would yield a severe loss

279 Rats were administered 6-hydroxydopamine to induce brainstem lesions, causing acu

280 ons, we have used the selective neurotoxin 6-hydroxydopamine to lesion their terminals within the str

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

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

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

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

285 for mitochondrially derived superoxide in 6-hydroxydopamine toxicity.

286 n the dyskinetic animals compared with the 6-hydroxydopamine-treated and control rats.

287 rded from the basal ganglia of control and 6-hydroxydopamine-treated hemi-parkinsonian rats anestheti

288 l models of DA neuron loss and PD, such as 6-hydroxydopamine-treated mice or rats and 1-methyl-4-phen

289 ntation of these cells into the striata of 6-hydroxydopamine-treated rats at the neuronal progenitor

290 potassium removal, glutamate toxicity, or 6-hydroxydopamine treatment and found that clone 17a trans

291 ture and prevents their degeneration after 6-hydroxydopamine treatment in vivo.

292 was ablated by chemical sympathectomy with 6-hydroxydopamine treatment.

293 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 dopa

295 eriment 1, rats received microinfusions of 6-hydroxydopamine unilaterally to induce dopamine terminal

296 ion produced by intrastriatal injection of 6-hydroxydopamine was indistinguishable between WT and A(2

297 lexiform 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 i

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

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