ライフサイエンスコーパス: MPTP

1 MPTP (0-0.31 mg/kg) infused unilaterally via the interna

2 MPTP exacerbated these effects, with the lowest density

3 MPTP gave rise to increased locomotion, regardless of ge

4 MPTP injections (1.5-2.1mg/kg) were made over a 5- to 7-

5 MPTP treatment also induced mitochondrial translocation

6 MPTP was determined using the calcein-cobalt technique.

7 MPTP-induced microglial activation and astrogliosis were

8 MPTP-induced reductions in ferroportin and elevations in

9 MPTP-lesioned primates were given systemic C3 (n = 8) or

10 MPTP-mediated toxicity in primary dopaminergic neurons w

11 it was not present in Macaca fascicularis (7 MPTP and 8 controls) with similar degree of MPTP-induced

12 ptide inhibitor P110 is neuroprotective in a MPTP animal model.

13 Inflammation induces aberrant MPTP opening, resulting in an increased apoptosis in con

14 Accordingly, MPTP/MPP(+) (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridin

15 nsitizes pancreatic mitochondria to activate MPTP, leading to mitochondrial failure; this makes the p

16 Ethanol and CCK activated MPTP through different mechanisms-ethanol by reducing th

17 antagonist KW-6002 but did not affect acute MPTP neurotoxicity.

18 tant components for protection against acute MPTP toxicity.

19 out mice reinstated protection against acute MPTP-induced dopaminergic neurotoxicity and attenuated M

20 administration of NTZ (50 mg/kg) in an acute MPTP mouse model of PD conferred significant protection

21 cise potently protects DA neurons from acute MPTP toxicity, suggesting that this simple lifestyle ele

22 persistent and progressive disease in acute MPTP-intoxicated mice.

23 atal pathologies do not persist in the acute MPTP mouse model.

24 rain penetrant c-Abl inhibitor, in the acute MPTP-induced model of PD.

25 Additional MPTP injections resulted in the association of a severe

26 oups of adult C57BL/6 mice were administered MPTP with varying subcutaneous or oral dosing regimens o

27 ) and Nrf2(-/-) background were administered MPTP.

28 ly, mice treated with allopregnanolone after MPTP lesion were able to perform at levels similar to th

29 striatum and improved gait dysfunction after MPTP administration.

30 s and lowered striatal dopamine levels after MPTP treatment, an effect that was reversed by selective

31 was determined by stereological tests after MPTP intoxication in mice pretreated with either VIPR1 o

32 nd mitochondrial translocation in vivo after MPTP administration.

33 o (n = 7) for 2 months starting 1 week after MPTP.

34 for their abilities to protect mice against MPTP-induced neurodegeneration used to model Parkinson's

35 that are potentially neuroprotective against MPTP and that these factors change over time.

36 astrocytes is sufficient to protect against MPTP and astrocytic modulation of the Nrf2-ARE pathway i

37 , these data suggest that protection against MPTP neurotoxicity may be mediated by alterations in iro

38 xercise provided complete protection against MPTP-induced neurotoxicity.

39 myeloid cells significantly protects against MPTP neurotoxicity and preserves striatal dopamine level

40 inergic cells and their terminations against MPTP insult, particularly in animals that developed few

41 e a key factor in protecting the VTA against MPTP-induced cell death, and that exogenous application

42 esides solely upon the soluble isoform in an MPTP-induced model of Parkinson's disease.

43 ue to follow this degeneration process in an MPTP-induced mouse model of PD.

44 stribution in response to Homer deletion and MPTP lesion.

45 en dysfunctional microglia of aging mice and MPTP exposure further inhibited astrocyte proneurogenic

46 by comparing glutamate levels in normal and MPTP-lesioned nonhuman primates (Macaca mulatta).

47 electron microscopic approach in normal and MPTP-treated monkeys.

48 of multisynaptic connectivity in normal and MPTP-treated monkeys; and 3) VGluT1- and vGluT2-positive

49 igra pars compacta (SNpc) against 6-OHDA and MPTP.

50 ndria exhibiting both IMAC-mediated RIRR and MPTP-mediated RIRR, diffusively coupled in a spatially e

51 ) lesion model of drug-induced rotation, and MPTP-treated non-human primate model.

52 neuron loss, and inflammatory phenotypes as MPTP-treated CX3CL1(-/-) mice, which received the GFP-ex

53 dministration of SB216763 and atractyloside (MPTP opener) failed to abrogate a local cytoprotective G

54 ed dopaminergic neurotoxicity and attenuated MPTP-induced striatal microglial and astroglial activati

55 Independent of background, MPTP-mediated toxicity was abolished in GFAP-Nrf2 mice.

56 a selective peptide inhibitor P110, blocked MPTP-induced Drp1 mitochondrial translocation and attenu

57 evented IOBA-NHC from cell death by blocking MPTP opening, DeltaPsim loss, Fas/FasL, and caspase acti

58 /-) mice were much more severely affected by MPTP than were those of their WT littermates.

59 nal damage and behavioral deficits caused by MPTP.

60 opening, or bistable dynamics facilitated by MPTP opening; 2), in a diffusively-coupled mitochondrial

61 ted the DAergic neurodegeneration induced by MPTP or 1-methyl-4-phenyl-pyridium iodide (MPP(+)) expos

62 effects of ethanol and CCK were mediated by MPTP because they were not observed in CypD(-/-) acinar

63 In PMA/alphaCD3-activated Jurkat T cells, MPTP opening and DeltaPsim loss were increased along wit

64 halted the disease progression in a chronic MPTP mouse model.

65 ow that neurodegeneration induced by chronic MPTP regimen is prevented by genetic deletion of SIRT2 i

66 In this study, using a classical MPTP animal PD model, we showed for the first time Drp1

67 maintaining the hydrogen bond; in contrast, MPTP*+ + tBu3PhOH maintains its conformation throughout

68 Furthermore, Nur77-deficient MPTP-treated mice displayed significantly reduced levels

69 PTP*+ < DeltaG()PPT*+ despite DeltaG degrees MPTP*+ > DeltaG degrees PPT*+.

70 oth experiment and calculations with DeltaG()MPTP*+ < DeltaG()PPT*+ despite DeltaG degrees MPTP*+ > D

71 Drp1 mitochondrial translocation diminished MPTP-induced p53, BAX and PUMA mitochondrial translocati

72 ivation of astrocytes stimulated by low-dose MPTP and inflammatory cytokines.

73 acids that occurs by a novel pathway during MPTP formation.

74 Genetic deficiency of the CIB1 gene enhances MPTP-induced neurotoxicity in dopaminergic neurons in CI

75 mutants lacking PGRN in microglia exhibited MPTP-induced phenotypes similar to Grn(-)/(-) mice.

76 Following MPTP or vehicle administration, mice ran on the treadmil

77 movement-related activity declined following MPTP but only marginally.

78 euron loss and behavioral deficits following MPTP intoxication.

79 nd its metabolites (DOPAC and HVA) following MPTP treatment as determined by HPLC method.

80 ost significant numbers of neurons following MPTP administration as compared to saline treated mice;

81 beled neurons/section in the SN-PC following MPTP, treadmill exercise leads to an increase of neurons

82 After controlling for MPTP-induced changes in motor performance, M1 activity r

83 cise also functionally protects neurons from MPTP-induced neurotoxicity.

84 release of dopamine and neuroprotection from MPTP toxicity in the VMAT2-overexpressing mice suggest t

85 trocytic Nrf2 overexpression to protect from MPTP toxicity.

86 inflammatory cytokine release resulting from MPTP exposure.

87 hydrogenase mRNA and activity resulting from MPTP were also found to be attenuated by DHB.

88 The present study exposed monkeys to higher MPTP doses to produce significant parkinsonism and behav

89 The effects of allopregnanolone in MPTP-lesioned mice were more apparent in mice that under

90 -) mice was associated with an alteration in MPTP-mediated Ca(2+) efflux resulting in elevated levels

91 increased volume of their spine apparatus in MPTP-treated monkeys, suggesting an increased protein sy

92 rotect against nigrostriatal degeneration in MPTP-intoxicated mice.

93 okines, did not induce persistent disease in MPTP-insulted mice.

94 correlates with their protective efficacy in MPTP-mediated neurotoxicity.

95 continuous impairment of motor functions in MPTP-intoxicated mice.

96 ransmitters, and improved motor functions in MPTP-intoxicated mice.

97 ransmitters, and improved motor functions in MPTP-intoxicated mice.

98 ransmitters, and improved motor functions in MPTP-intoxicated mice.

99 A role for NF-kappaB in MPTP-dependent induction of NOS1 was confirmed through o

100 Adding bilateral PPN lesions in MPTP-lesioned macaques induced dopamine-resistant gait a

101 s sensorimotor territory) was 26.1% lower in MPTP-treated parkinsonian monkeys than in controls.

102 ponses and protected dopaminergic neurons in MPTP-intoxicated mice, but at levels less than simvastat

103 FTI and GGTI also protected nigrostriata in MPTP-intoxicated mice.

104 essed NO production and protein nitration in MPTP-activated astrocytes and completely protected cocul

105 e response of SVZ neuroprogenitors (NPCs) in MPTP-treated mice.

106 e components of the nigrostriatal pathway in MPTP-lesioned mice by measuring striatal dopamine levels

107 tal tract, improves the motor performance in MPTP-treated mice, and may serve as a therapeutic strate

108 yperdirect cortico-subthalamic projection in MPTP-treated parkinsonian monkeys.

109 suggest that CIB1 plays a protective role in MPTP/MPP(+)-induced neurotoxicity by blocking ASK1-media

110 monstrate that MAC1 plays a critical role in MPTP/MPP(+)-induced reactive microgliosis and further su

111 flammation and Wnt/beta-catenin signaling in MPTP-induced loss and repair of nigrostriatal dopaminerg

112 ation of neuronal cell bodies and termini in MPTP-intoxicated mice.

113 d exposure to environmental toxins including MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) are

114 nd Nrf2(-/-) mice; Nrf2 deficiency increases MPTP sensitivity.

115 hereas ER-Nix activates Bax/Bak-independent, MPTP-dependent necrosis.

116 In IOBA-NHC, TNFalpha, and IFNgamma induced MPTP opening, DeltaPsim loss, and increased cell apoptos

117 stimulated with thapsigargin, which induces MPTP formation by a direct effect on mitochondria, LDH a

118 e deletion of CD95 in DNs does not influence MPTP-induced neurodegeneration.

119 tochondrial calcium uptake but by inhibiting MPTP formation.

120 After transplantation into MPTP-lesioned mice, iDPs differentiated into DA neurons,

121 for 5 days and killed 7 days after the last MPTP injection.

122 conductance without altering inner membrane MPTP function, resulting in resistance to mitochondrial

123 and 16 were orally active in vivo in a mouse MPTP biochemical efficacy model that was comparable to t

124 NO suppresses APP translation in mouse MPTP models, explaining how elevated NO causes iron-depe

125 the parkinsonism-inducing neurotoxin MPP(+)/MPTP model that alpha-Synuclein (alpha-Syn), a presynapt

126 ta), is robustly activated in various MPP(+)/MPTP models of Parkinsonism (SH-SY5Y cotransfected cells

127 urons and several DA cell lines against MPP+/MPTP.

128 lly capable of activating the pro-neurotoxin MPTP and inducing neuronal damage, which is effectively

129 tic inflammatory responses to the neurotoxin MPTP and reduced striatal dopamine turnover.

130 Furthermore, exposure to the neurotoxin MPTP depleted neurons in the ventrolateral VTA and resul

131 sly administered low doses of the neurotoxin MPTP over several months to produce cognitive deficits,

132 mates, and certain rodents by the neurotoxin MPTP.

133 lpha overexpression alone, in the absence of MPTP treatment, did not lead to cell loss in the SN or t

134 duction of parkinsonism by administration of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and

135 Chronic administration of MPTP induces lesion via apoptosis.

136 Intraperitoneal administrations of MPTP (a neurotoxin) were delivered to mice at regular in

137 ivo in the substantia nigra pars compacta of MPTP-intoxicated mice.

138 with low or 'sub-optimal' concentrations of MPTP (1 microM) and the inflammatory cytokine tumor necr

139 f T cells into the nigra was found on 1 d of MPTP insult, T cell infiltration decreased afterward, be

140 MPTP and 8 controls) with similar degree of MPTP-induced nigrostriatal neurodegeneration; and (4) DA

141 striatum before and after a variable dose of MPTP in nonhuman primates.

142 e VTA to sustained exposure to a low dose of MPTP.

143 cillations, whereas the bistable dynamics of MPTP-mediated RIRR results in slow (0.1-2 microm/s) PsiM

144 urons in the substantia nigra independent of MPTP treatment, suggesting that microglial EP2 may influ

145 ase was developed using staged injections of MPTP.

146 , can efficiently catalyze the metabolism of MPTP to MPP(+), as shown with purified enzymes and also

147 discovery of the selective neurotoxicity of MPTP to dopamine cells, suspicion has focused on paraqua

148 ve synthesized and characterized a number of MPTP and MPP(+) derivatives that are suitable for the co

149 uces a functional response in the outcome of MPTP-induced DAergic toxicity.

150 e of glial cells, catalyzes the oxidation of MPTP to the toxic 1-methyl-4-phenylpyridinium ion (MPP(+

151 a fundamental role in the physiopathology of MPTP-induced PD in a mouse model.

152 alone are also maintained in the presence of MPTP.

153 vestigate the role of Nrf2 in the process of MPTP-induced toxicity, mice expressing the human placent

154 To examine the role of MPTP, we used ex vivo and in vivo models of pancreatitis

155 sitive and total cell numbers in the SNpc of MPTP-lesioned mice, even though this did not increase st

156 igand binding was evident in the striatum of MPTP lesioned animals as compared with the control group

157 caspase activities with a minimal effect on MPTP.

158 nistration, mice were treated with saline or MPTP.

159 or 3months prior to treatment with saline or MPTP.

160 or 3months prior to treatment with saline or MPTP.

161 MCU-mediated mitochondrial calcium overload, MPTP formation, and necrotic cell death.

162 ted the effects of ethanol on the pancreatic MPTP, the mechanisms of these effects, and their role in

163 wo toxin models of Parkinson's disease (PD), MPTP and paraquat, in young animals, its prolonged eleva

164 hance outer membrane permeability, permitted MPTP-dependent mitochondrial swelling and restored necro

165 -(pyrid-2-yl)-10-methyl-10H-phenothiazinium (MPTP*+).

166 c loss following 1-methyl-4-phenylpyridinium/MPTP treatment, in vitro and in vivo.

167 mitochondrial permeability transition pore (MPTP) causes loss of the mitochondrial membrane potentia

168 mitochondrial permeability transition pore (MPTP) causes loss of the mitochondrial membrane potentia

169 mitochondrial permeability transition pore (MPTP) causes mitochondrial dysfunction and necrosis in a

170 mitochondrial permeability transition pore (MPTP) formation, lactate dehydrogenase (LDH) release, an

171 mitochondrial permeability transition pore (MPTP) opening.

172 mitochondrial permeability transition pore (MPTP) via cyclophilin D and p53 as mechanisms of EPHOSS.

173 Mitochondrial Permeability Transition Pore (MPTP), is formed within the c-subunit ring of the ATP sy

174 mitochondrial permeability transition pore (MPTP).

175 mitochondrial permeability transition pore (MPTP).

176 mitochondrial permeability transition pore (MPTP).

177 mitochondrial permeability transition pore (MPTP).

178 mitochondria permeability transition pores (MPTP).

179 n was restored to normal within 1 month post-MPTP in BMT-treated mice assayed by a rotarod behavioral

180 +) uniporter (MCU) regulator, also prevented MPTP formation and arachidonic acid release induced by A

181 ting myeloid cells, and efficiently prevents MPTP-induced DN death.

182 We used the progressively MPTP-intoxicated monkey model that expresses recovery fr

183 onal and unique benefit in mice who received MPTP.

184 a knockdown or GSK-3beta antagonism reversed MPTP-induced neurogenic impairment ex vivo/in vitro or i

185 The same MPTP protocol was applied in Nrf2(+/+) and Nrf2(-/-) mic

186 nt sensitivity to damage induced by systemic MPTP treatment.

187 4-(2'-methylphenyl)-1,2,3,6-tetrahydrophine (MPTP), mice lacking PGRN (Grn(-)/(-)) showed more neuron

188 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP)-induced neurodegeneration using tissue-specific de

189 -methyl-4-phenyl-1,2,5,6 tetrahydropyridine (MPTP) treatment.

190 -methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP).

191 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration affected extracellular cortical glu

192 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and dyskinetic with levodopa.

193 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of PD.

194 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) caused dopaminergic cell death.

195 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposure in nonhuman primates.

196 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the adult mouse.

197 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into non-human primates causes injury to the nigro

198 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication to model PD in mice.

199 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication to render them parkinsonian and then

200 -Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a dopaminergic neurotoxin that replicates most

201 -Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxic side product formed in the chemica

202 thyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) model of Parkinson's disease (PD).

203 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease.

204 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease.

205 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD to investigate the possible use of LXR

206 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD.

207 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model is the most widely used animal model f

208 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease (PD).

209 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease.

210 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on locomotion and DA neurons in 26-month-old male

211 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) through a mechanism distinct from that described f

212 -methyl 4-phenyl 1,2,3,6-tetrahydropyridine (MPTP) toxicity.

213 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment in vivo, Nur77 expression in the nigrost

214 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), abnormal low beta (8-15 Hz) spiking and local fie

215 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), as measured by reduced dopamine terminal damage a

216 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), leading to parkin inactivation, accumulation of t

217 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), N-methyl-4-phenylpyridinium (MPP(+)), selectively

218 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which induces selective neuronal loss in the midb

219 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced bilateral nigrostriatal dopaminergic lesio

220 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigral dopaminergic cell loss and up-regul

221 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model.

222 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD.

223 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice where it inhibits parkin through

224 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice.

225 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated monkeys (when motor symptoms are less

226 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mice.

227 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse.

228 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mediated cell death of dopaminergic neurons in the

229 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-rendered Parkinsonian nonhuman primate model of l-

230 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys, as well as in some electrophysiol

231 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys.

232 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated nonhuman primates.

233 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

234 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

235 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

236 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

237 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

238 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP/MPP+) in a mouse model of PD.

239 l and Western blot studies demonstrated that MPTP/MPP(+) produced less microglia activation in MAC1(-

240 It was also noted that MPTP treated mice to which allopregnanolone was administ

241 In conclusion, our findings suggest that MPTP induced PD in mouse model is appropriate to follow

242 The MPTP inhibitor cyclosporin A protects mouse bone marrow

243 or function despite administration after the MPTP injury process had begun.

244 Combined inhibition of caspases and the MPTP fully protected against Nix-mediated cell death.

245 CR attenuated the MPTP-induced loss of substantia nigra (SN) dopamine neur

246 By contrast, the MPTP-NIr group developed much less clinical and behavior

247 by suggesting a physiologic function for the MPTP.

248 D on the development of the phenotype in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinen) mod

249 All monkeys in the MPTP group developed severe clinical and behavioral impa

250 , and as a result, enhances apoptosis in the MPTP model of PD.

251 synthase (NOS1) in both human PD and in the MPTP model of the disease.

252 Furthermore, juglone treatment in the MPTP mouse model of PD suppressed Pin1 levels and improv

253 persistent nigrostriatal pathologies in the MPTP mouse model, and that targeting these factors may h

254 down the progression of neuronal loss in the MPTP mouse model.

255 APP-overexpressing mice are protected in the MPTP PD model.

256 Further, in the MPTP-induced neurotoxin model of PD in cultured cells an

257 r to 1-methyl-4-phenylpyridinium (MPP+), the MPTP metabolite responsible for its neurotoxicity.

258 cell death, the physiologic function of the MPTP is largely unknown.

259 molecular identity of the components of the MPTP remains unknown.

260 in cyclophilin D (CypD), a component of the MPTP, are resistant to MPTP opening, loss of DeltaPsim,

261 tion waves; and 3), the slow velocity of the MPTP-mediated depolarization wave is related to competit

262 ilitating outer membrane permeability of the MPTP.

263 peptidyl-prolyl isomerase that regulates the MPTP and is a drug target for AP.

264 Our data predict that the MPTP is an inner membrane regulated process, although in

265 These findings suggest that the MPTP maintains homeostatic mitochondrial Ca(2+) levels t

266 motor cortex on the side ipsilateral to the MPTP-lesion.

267 re inconsistent with those attributed to the MPTP.

268 immunocytes or natural Tregs administered to MPTP mice attenuated microglial inflammatory responses a

269 ns from agonist-treated mice administered to MPTP-intoxicated animals.

270 rm provides no neuroprotective capability to MPTP-induced pathologies, exhibiting similar motor coord

271 ost significant numbers of DA neurons due to MPTP toxicity; however, the 2/3 running group demonstrat

272 se in TH-labeled neurons in the SN-PC due to MPTP will be partially reversed by treadmill exercise, l

273 que transcriptional response when exposed to MPTP, a neurotoxin able to mimic the selective cell loss

274 icient for neuroprotection after exposure to MPTP.

275 Administration of the LXR agonist GW3965 to MPTP-treated WT mice protected against loss of dopaminer

276 eptibility of LRRK2 KO and wild-type mice to MPTP.

277 ctive vulnerability of Grn(-)/(-) neurons to MPTP, but rather to an increased microglial inflammatory

278 role in the susceptibility of DA neurons to MPTP, we generated LRRK2 knock-out (KO) mice lacking the

279 ired for the susceptibility of DA neurons to MPTP.

280 ), a component of the MPTP, are resistant to MPTP opening, loss of DeltaPsim, and necrosis.

281 h are devoid of T cells and are resistant to MPTP-induced neurodegeneration, become susceptible to MP

282 ression of 148 genes as an early response to MPTP and 113 genes as a late response to MPTP toxicity.

283 and subsequent neurotoxicity in response to MPTP intoxication.

284 to MPTP and 113 genes as a late response to MPTP toxicity.

285 tionally increased in the VTA in response to MPTP.

286 drion-targeted CYP2D6 were more sensitive to MPTP-mediated mitochondrial respiratory dysfunction and

287 -1alpha also led to increased sensitivity to MPTP-induced death of Th+ neurons.

288 vels of Pitx3 and enhances susceptibility to MPTP.

289 ced neurodegeneration, become susceptible to MPTP-induced loss of dopaminergic neurons when reconstit

290 ly, D3R-deficient mice become susceptible to MPTP-induced neurodegeneration and microglial activation

291 pronounced effects in VIPR2 agonist-treated, MPTP-intoxicated mice.

292 Unilateral MPTP-administration rendered the animals with hemiparkin

293 PRP activity was elevated in the untreated MPTP hemispheres relative to those of the normal control

294 activity remained unchanged in the untreated MPTP hemispheres versus the sham-operated hemispheres.

295 Importantly, in vivo studies using MPTP, LPS, or 6-OHDA models revealed a greater attenuati

296 lar results in aged monkeys intoxicated with MPTP: they developed severe DOPA-responsive hypokinesia

297 hydroxylase expression after lesioning with MPTP.

298 al mouse and after damage of DA neurons with MPTP.

299 Pre-exposure to CD to mice treated with MPTP resulted in an exacerbation of motor deficit and a

300 d nigrostriatal damage when compared with WT MPTP-treated controls.