ライフサイエンスコーパス: nigrostriatal

1 insonian-like motor deficits in a unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) lesion model us

2 n, and sensorimotor neglect after unilateral nigrostriatal 6-hydroxydopamine lesion in mice.

3 Here, we show that phasic activation of nigrostriatal afferents in a mouse striatal slice prepar

4 The nigrostriatal and histological perspectives are not inco

5 of intravenous cocaine, and dopamine in both nigrostriatal and mesocorticolimbic terminal fields part

6 y tracing viruses simultaneously illuminates nigrostriatal and mesolimbic circuitry and shows no over

7 Thus, the similarities between nigrostriatal and mesolimbic dopamine systems can be as

8 The anatomical evidence for independent nigrostriatal and mesolimbic dopamine systems has, howev

9 tions are responsible for the segregation of nigrostriatal and mesolimbic dopaminergic pathways.

10 Nigrostriatal and ventral tegmental area (VTA) midbrain

11 al microglial activation, protected both the nigrostriatal axis and neurotransmitters, and improved m

12 progressing to bilateral degeneration of the nigrostriatal axis with aging.

13 e development of degenerative changes in the nigrostriatal axons and terminals.

14 ilarly, neither unilateral 6-OHDA lesions of nigrostriatal axons nor the dorsal noradrenergic bundle

15 or parkinsonism with the degree of injury to nigrostriatal axons, as reflected by in vitro fiber leng

16 responsive dystonia, but also predisposes to nigrostriatal cell loss.

17 in severe reduction of dopamine synthesis in nigrostriatal cells and are the most common cause of DOP

18 essential enzyme for dopamine production in nigrostriatal cells.

19 ease and striatal synaptic plasticity in the nigrostriatal circuit and suggest that altered dopaminer

20 ial striatum (DMS) and midbrain areas of the nigrostriatal circuit are critically associated to strok

21 l and electrophysiological properties of the nigrostriatal circuit in behaviorally asymptomatic 6- to

22 or behavior, but growing data implicate this nigrostriatal circuit in emotion.

23 rochemical and structural homeostasis in the nigrostriatal circuit.

24 Mfn1 yielded no corresponding defects in the nigrostriatal circuit.

25 e widely used to produce degeneration of the nigrostriatal circuitry.

26 tain an outcome, we found neural activity in nigrostriatal circuits specifically signalling the initi

27 rpose of this study was to determine whether nigrostriatal DA depletion affects measures of insulin r

28 r, these results support the hypothesis that nigrostriatal DA depletion impairs insulin signaling in

29 Here we investigated the role of nigrostriatal DA in fear extinction.

30 abnormality promoting mechanisms leading to nigrostriatal DA neuron death in PD.

31 st that neurons other than or in addition to nigrostriatal DA neurons contributed to protection of fo

32 cteristic electrophysiological properties of nigrostriatal DA neurons, produce high levels of dopamin

33 can contribute to the preferential death of nigrostriatal DA neurons.

34 These data suggest that in nigrostriatal DA pathway, chronic nicotine enhancement o

35 5-HT upregulation following the loss of the nigrostriatal DA projection and that the upregulated 5-H

36 ely in identified mesolimbic DA VTA, but not nigrostriatal DA SN, neurons.

37 to assess toxic challenges of the developing nigrostriatal DA system, in vitro.

38 2 elicits its neuroprotective effects on the nigrostriatal DA system.

39 Nigrostriatal DA thus represents a novel target to enhan

40 s a mechanism by which DAT and Oct3 modulate nigrostriatal damage induced by PQ(2+)/PQ(+) redox cycli

41 this, we investigated the effect of varying nigrostriatal damage on alpha6beta2* and alpha4beta2* re

42 r is decreased to a much greater extent with nigrostriatal damage than the alpha4beta2* subtype raisi

43 aptic FosB activity, indicative of increased nigrostriatal damage when compared with WT MPTP-treated

44 ecreased to a similar extent with increasing nigrostriatal damage, indicating that both subtypes cont

45 population is more important with increased nigrostriatal damage.

46 release also decreased proportionately with nigrostriatal damage.

47 rbations of mitochondrial dynamics can cause nigrostriatal defects and may be a risk factor for the n

48 esterol-lowering drug, could protect against nigrostriatal degeneration after 1-methyl-4-phenyl-1,2,3

49 T mutant alpha-synuclein induced progressive nigrostriatal degeneration and reduced locomotion.

50 uroregulatory activities affect the tempo of nigrostriatal degeneration during Parkinson's disease (P

51 Symptomatic models of PD based on nigrostriatal degeneration have a high degree of predict

52 his model may provide insight into selective nigrostriatal degeneration in human IBGC and other Parki

53 of RANTES and eotaxin could protect against nigrostriatal degeneration in MPTP-intoxicated mice.

54 minergic terminals particularly sensitive to nigrostriatal degeneration in Parkinson's disease.

55 This study investigated the extent of nigrostriatal degeneration in patients with Parkinson's

56 mechanism by which loss of PINK1 may lead to nigrostriatal degeneration in PD.

57 itopes that exacerbate neuroinflammation and nigrostriatal degeneration in the 1-methyl-4-phenyl-1,2,

58 inase alpha (IKKalpha) or IKKbeta to prevent nigrostriatal degeneration in the 1-methyl-4-phenyl-1,2,

59 cate that IFN-gamma mediates age-progressive nigrostriatal degeneration in the absence of exogenous s

60 s of MEF2 activity, plays a critical role in nigrostriatal degeneration in vivo.

61 Thus, VMAT2 LO animals display nigrostriatal degeneration that begins in the terminal f

62 The pace of nigrostriatal degeneration, both with regards to striata

63 l plasticity, which, in the absence of overt nigrostriatal degeneration, suggest there are age-relate

64 thic basal ganglia calcification (IBGC), and nigrostriatal degeneration.

65 nd natural Tregs reversed N-alpha-syn T cell nigrostriatal degeneration.

66 e substantia nigra pars compacta, leading to nigrostriatal degeneration.

67 phosphorylation eliminates alpha-syn-induced nigrostriatal degeneration.

68 proteasome inhibitor (lactacystin) -induced nigrostriatal degeneration.

69 physiology may be a pathogenic precursor to nigrostriatal degeneration.

70 hite matter signal hyperintensity burden and nigrostriatal denervation as independent variables demon

71 Acute trkB blockade in rats with stable nigrostriatal denervation attenuated the forelimb akines

72 Nigrostriatal denervation did not affect SVZ proliferati

73 f significant cerebral amyloid deposition or nigrostriatal denervation was a strong predictor of conv

74 hesized that factors highly expressed during nigrostriatal development and re-expressed after injury

75 natal LPS exposure, and in vitro analysis of nigrostriatal development in organotypic cultures prepar

76 Such alterations in nigrostriatal development may demonstrate how adverse pe

77 nization of behaviour, and is compromised in nigrostriatal disorders like Parkinson's and Huntington'

78 f insulin resistance and the degeneration of nigrostriatal dopamine (DA) neurons are both mediated by

79 The cause of degeneration of nigrostriatal dopamine (DA) neurons in idiopathic Parkin

80 Progressive loss of nigrostriatal dopamine (DA) neurons is the neuropatholog

81 's disease (PD) involves progressive loss of nigrostriatal dopamine (DA) neurons over an extended per

82 neration of a unique population of cells-the nigrostriatal dopamine (DA) neurons-that occurs in Parki

83 ase (PD) is characterized by degeneration of nigrostriatal dopamine (DA) neurons.

84 Recent data suggest that lesions of nigrostriatal dopamine axons cause a loss of PF neurons,

85 Here we demonstrate that nigrostriatal dopamine biases ongoing action selection.

86 a neurodegenerative disease characterized by nigrostriatal dopamine damage and gliosis.

87 the existence of compensatory mechanisms in nigrostriatal dopamine degeneration and provide new insi

88 cell loss in parkinsonism is independent of nigrostriatal dopamine degeneration.

89 is a primary event rather than secondary to nigrostriatal dopamine degeneration.

90 Unilateral nigrostriatal dopamine depletion also causes a contralat

91 Unilateral nigrostriatal dopamine depletion in animals induces cont

92 Sustained nigrostriatal dopamine depletion increases the serine/th

93 These data confirm that nigrostriatal dopamine depletion is accompanied by profo

94 stantia nigra pars compacta, suggesting that nigrostriatal dopamine dysfunction precedes detectable p

95 in the maintenance and protection of normal nigrostriatal dopamine function by activating UCP2-depen

96 These results unveil a crucial role of nigrostriatal dopamine in integrating diverse informatio

97 aintain intact cognitive performance despite nigrostriatal dopamine loss.

98 Nigrostriatal dopamine neuron lesions did not elicit deg

99 ive disorder pathologically characterized by nigrostriatal dopamine neuron loss and the postmortem pr

100 However, even when nigrostriatal dopamine neuron loss is severe enough to c

101 We identify two parallel nigrostriatal dopamine neuron subpopulations differing i

102 SNCA-OVX mice display age-dependent loss of nigrostriatal dopamine neurons and motor impairments cha

103 y be related to the initial pathology of the nigrostriatal dopamine neurons and resulting dopamine de

104 Recent evidence indicates that nigrostriatal dopamine neurons inhibit striatal projecti

105 ss of the PPTg with bilateral destruction of nigrostriatal dopamine neurons that mimics human pathoph

106 erent time points, changes in firing rate of nigrostriatal dopamine neurons, as well as dopamine sign

107 hemical or anatomical evidence of lesions of nigrostriatal dopamine neurons, nor were any changes in

108 causes a slowly progressive degeneration of nigrostriatal dopamine neurons, the presence of inclusio

109 erative disorder that results in the loss of nigrostriatal dopamine neurons.

110 d in vitro and in vivo the effects of PSI on nigrostriatal dopamine neurons.

111 isease (PD) is mainly due to degeneration of nigrostriatal dopamine neurons.

112 ciated not only with the degeneration of the nigrostriatal dopamine neurotransmission, but also with

113 Our findings suggest that the nigrostriatal dopamine pathway is involved to some exten

114 but not at the origins of the mesolimbic and nigrostriatal dopamine pathways; no detectable level of

115 ia since their activation reduces mesolimbic nigrostriatal dopamine release (which conveys antipsycho

116 Lesions of the rat nigrostriatal dopamine system by injection of 6-hydroxyd

117 chloroethylene exposure is neurotoxic to the nigrostriatal dopamine system that degenerates in Parkin

118 tudents of Parkinson's disease who study the nigrostriatal dopamine system that originates in the sub

119 diated toxicity and neurodegeneration in the nigrostriatal dopamine system.

120 food addiction indicates that mesolimbic and nigrostriatal dopamine systems often are cited as mechan

121 This article gives an update on nigrostriatal dopamine terminal imaging, with emphasis o

122 G) structures also revealed a major role for nigrostriatal dopamine, the striatum, and the external g

123 -stage Parkinson's disease (PD) with reduced nigrostriatal dopamine, whereas, asymptomatic carriers h

124 ine on functional alpha4beta2* nAChRs in the nigrostriatal dopaminergic (DA) pathway.

125 In animal models of PD, E2 protects the nigrostriatal dopaminergic (DA) system against neurotoxi

126 signaling in MPTP-induced loss and repair of nigrostriatal dopaminergic (DAergic) neurons prompted us

127 We conclude that 5-HT(2C)Rs regulate nigrostriatal dopaminergic activity and function both at

128 ion regulates PKCdelta expression to augment nigrostriatal dopaminergic cell death, which could contr

129 igate the physiological role of PINK1 in the nigrostriatal dopaminergic circuit through the generatio

130 stress responses to better understand how a nigrostriatal dopaminergic deficit increases the prevale

131 Three weeks later, after behavioral and nigrostriatal dopaminergic deficits had developed, rats

132 pamine toxic lesion and a genetic model with nigrostriatal dopaminergic deficits, we found that acute

133 Severe nigrostriatal dopaminergic degeneration occurs in DLB, b

134 four patients referred for the assessment of nigrostriatal dopaminergic degeneration were scanned usi

135 roved our understanding of events leading to nigrostriatal dopaminergic degeneration, and identificat

136 tor performance independent of the degree of nigrostriatal dopaminergic denervation in Parkinson's di

137 otor impairment independent of the degree of nigrostriatal dopaminergic denervation in Parkinson's di

138 s a more robust determinant of hyposmia than nigrostriatal dopaminergic denervation in subjects with

139 ects of both leucoaraiosis and the degree of nigrostriatal dopaminergic denervation on motor features

140 ic terminal loss in thalamus and cortex, and nigrostriatal dopaminergic denervation, on postural sens

141 ough not with differential serotoninergic or nigrostriatal dopaminergic denervation.

142 r determinant of axial motor impairment than nigrostriatal dopaminergic denervation.

143 atients, indicating Parkinson's disease-like nigrostriatal dopaminergic denervation.

144 atients with PD are associated with impaired nigrostriatal dopaminergic function resulting in abnorma

145 Through radiotracer-based imaging of nigrostriatal dopaminergic function, a specific class of

146 ssion or an indirect consequence of impaired nigrostriatal dopaminergic function.

147 We describe clinical, genetic and nigrostriatal dopaminergic imaging ([(123)I]N-omega-fluo

148 -tetrahydropyridine (MPTP)-induced bilateral nigrostriatal dopaminergic lesions after unilateral puta

149 hyperactivation in vivo and in vitro rescues nigrostriatal dopaminergic neurodegeneration induced by

150 Pit3x-deficient mice, a model for selective nigrostriatal dopaminergic neurodegeneration, we tested

151 DLS infarction evoked abnormal plasticity in nigrostriatal dopaminergic neurons and DMS D1-neurons, c

152 Although the gross anatomy of the nigrostriatal dopaminergic neurons was normal in DRD mic

153 e (PD) is characterized primarily by loss of nigrostriatal dopaminergic neurons, there is a concomita

154 is metabolite produces rapid degeneration of nigrostriatal dopaminergic neurons, which causes the par

155 interact together to influence the number of nigrostriatal dopaminergic neurons.

156 cterized by a profound and selective loss of nigrostriatal dopaminergic neurons.

157 s in accelerated age-related degeneration of nigrostriatal dopaminergic neurons.

158 D) is characterized by a progressive loss of nigrostriatal dopaminergic neurons.

159 order characterized by a progressive loss of nigrostriatal dopaminergic neurons.

160 Diminished nigrostriatal dopaminergic neurotransmission is a bioche

161 es a reliable and reproducible lesion of the nigrostriatal dopaminergic pathway and neurodegeneration

162 rized by the progressive degeneration of the nigrostriatal dopaminergic pathway and the emergence of

163 2 to key neuronal populations throughout the nigrostriatal dopaminergic pathway is consistent with th

164 eceptor subtype on functions mediated by the nigrostriatal dopaminergic pathway is less clear.

165 n inclusions precedes the involvement of the nigrostriatal dopaminergic pathway.

166 terized by a progressive degeneration of the nigrostriatal dopaminergic pathway.

167 ghout the rodent brain, including within the nigrostriatal dopaminergic pathway.

168 Toxic organic cations can damage nigrostriatal dopaminergic pathways as seen in most park

169 long the trajectory of mesocorticolimbic and nigrostriatal dopaminergic pathways.

170 f mDAs and the segregation of mesolimbic and nigrostriatal dopaminergic pathways.

171 hed dopamine release and axonal pathology of nigrostriatal dopaminergic projection.

172 alpha-synuclein conversion and deposition at nigrostriatal dopaminergic synapses in transgenic mice,

173 PD and has a pathophysiological role in the nigrostriatal dopaminergic system and suggest that modul

174 We attempted to monitor the nigrostriatal dopaminergic system in rats with positron

175 rly PD nonmotor symptoms with imaging of the nigrostriatal dopaminergic system offers a promising pat

176 xplained by a compensatory adaptation of the nigrostriatal dopaminergic system possibly due to decrea

177 sociated with neuroprotective effects in the nigrostriatal dopaminergic system.

178 ts operate in modulating the function of the nigrostriatal dopaminergic system.media-1vid110.1093/bra

179 ld) were tested using paradigms sensitive to nigrostriatal dysfunction.

180 and occipital cortical synaptic activity and nigrostriatal function than PD noncarriers.

181 This study demonstrates altered nigrostriatal function that precedes behavioral parkinso

182 e SN PET measures are relevant biomarkers of nigrostriatal function.

183 Additionally, the level of nigrostriatal functional connectivity predicted the leve

184 r GABA brake for nigral dopamine systems and nigrostriatal functions, and they raise important questi

185 Our results reveal independently operating nigrostriatal information streams, with implications for

186 mine transporter (CFT) within 2 months after nigrostriatal injury.

187 We next investigated the effect of nigrostriatal lesioning on these two striatal alpha6beta

188 ase, we found that behaviorally undetectable nigrostriatal lesions induced a significant disconnectio

189 tical drive to dMSNs decreases after partial nigrostriatal lesions producing no behavioral impairment

190 tic of rodents with lateral hypothalamic and nigrostriatal lesions.

191 ol consumption and to uncover the underlying nigrostriatal mechanism.

192 differentially regulates mesolimbic- versus nigrostriatal-mediated functions.

193 d the ventral tegmental area, which form the nigrostriatal, mesolimbic, and mesocortical pathways.

194 In vertebrates, dopamine is central to the nigrostriatal motor and mesolimbic reward systems.

195 -derived LB extracts resulted in progressive nigrostriatal neurodegeneration starting at striatal dop

196 ports diagnosis of a condition not involving nigrostriatal neurodegeneration such as Alzheimer's dise

197 Abnormal imaging indicates underlying nigrostriatal neurodegeneration, supportive of a diagnos

198 owly progressive axon-initiated dopaminergic nigrostriatal neurodegeneration.

199 lex I inhibition, followed by an age-related nigrostriatal neurodegeneration.

200 ontrols) with similar degree of MPTP-induced nigrostriatal neurodegeneration; and (4) DA efflux studi

201 cacy of the potent antioxidant C3 to salvage nigrostriatal neuronal function after 1-methyl-4-phenyl-

202 y required for survival of dopaminergic (DA) nigrostriatal neurons and protect them from toxic insult

203 at dopamine is critical for SVZ function and nigrostriatal neurons are the main suppliers of SVZ dopa

204 se durations, we found that mesoaccumbal and nigrostriatal neurons differ substantially in rebound pr

205 re, these results show that mesoaccumbal and nigrostriatal neurons display differential responses to

206 (PPE), and on the integrity of dopaminergic nigrostriatal neurons in hemiparkinsonian mice.

207 Loss of nigrostriatal neurons leading to dopamine depletion in t

208 reviously reported targeted gene transfer to nigrostriatal neurons using chimeric gC-glial cell line-

209 iata but not from contralateral striata when nigrostriatal neurons were transduced.

210 have emphasized degeneration of dopaminergic nigrostriatal neurons with consequent dysfunction of cor

211 g exposure to toxins that selectively remove nigrostriatal neurons, suggesting that dopamine is criti

212 ned the aphakia mouse, which is deficient in nigrostriatal neurons, we found no detrimental effect to

213 zation-induced delays in spiking relative to nigrostriatal neurons.

214 ts receptors are constitutively expressed on nigrostriatal neurons.

215 er for presynaptic terminals in dopaminergic nigrostriatal neurons.

216 They also showed nigrostriatal neurotransmission deficits that were manif

217 minergic tracer binding and the diagnosis of nigrostriatal parkinsonism, particularly PD.

218 r Parkinson's disease (PD), it is known that nigrostriatal pathologies do not persist in the acute MP

219 Reversal of nigrostriatal pathologies in castrated male mice by subc

220 in could hold the key for driving persistent nigrostriatal pathologies in the MPTP mouse model, and t

221 our results suggest that castration induces nigrostriatal pathologies via iNOS-mediated decrease in

222 ntransgenic animal model to study PD-related nigrostriatal pathologies, paving the way for easy drug

223 le of male sex hormone in castration-induced nigrostriatal pathology.

224 in-deficient (parkin-/-) mice do not display nigrostriatal pathway degeneration, suggesting that a ge

225 ges as a novel drug target for prevention of nigrostriatal pathway degeneration, the neuropathologica

226 neurons that project to the striatum in the nigrostriatal pathway express GDNF receptors, GFR alpha1

227 ved FGF signaling, which assures an adequate nigrostriatal pathway formation and target innervation.

228 In TH-Cre mice whose nigrostriatal pathway had been eliminated unilaterally w

229 in the restoration of the components of the nigrostriatal pathway in MPTP-lesioned mice by measuring

230 y of (18)F-FE-PE2I as a tool for imaging the nigrostriatal pathway in Parkinson disease (PD) with PET

231 nd for DAT quantification and imaging of the nigrostriatal pathway in PD.

232 into non-human primates causes injury to the nigrostriatal pathway including nigral cell bodies, axon

233 The progressive loss of the nigrostriatal pathway is a distinguishing feature of Par

234 placement of fetal striatal co-grafts in the nigrostriatal pathway might elicit neuritic outgrowth to

235 ovide further evidence that the dopaminergic nigrostriatal pathway plays a role in the modulation of

236 idbrain dopaminergic neurons project via the nigrostriatal pathway to the striatum to regulate volunt

237 biting a decrease in dopamine release in the nigrostriatal pathway, as measured with fast-scan cyclic

238 However, the influence of the tVTA on the nigrostriatal pathway, from the substantia nigra pars co

239 general and how it affects the dopaminergic nigrostriatal pathway, in particular.

240 n nucleus, and it innervates, apart from the nigrostriatal pathway, several motor-related areas.

241 al dopaminergic neurons and consequently the nigrostriatal pathway, which has been found to innervate

242 lpha- synuclein (hA53T-alpha-syn) in the rat nigrostriatal pathway, with or without treatment using t

243 th animals treated only with 6-OHDA into the nigrostriatal pathway.

244 , and functional lesions of the dopaminergic nigrostriatal pathway.

245 response to dopaminergic dysfunction of the nigrostriatal pathway.

246 s disease process, not just the dopaminergic nigrostriatal pathway.

247 rkinson's disease, suggesting defects in the nigrostriatal pathway.

248 ting a neuroprotective role for RGS10 in the nigrostriatal pathway.

249 nked to death of dopaminergic neurons in the nigrostriatal pathway.

250 striatal grafts (STR) 2.5 mm rostral in the nigrostriatal pathway.

251 or delay the progressive degeneration of the nigrostriatal pathway.

252 oject to the striatum as part of the classic nigrostriatal pathway.

253 lease from the terminals of the dopaminergic nigrostriatal pathway.

254 y of (18)F-FE-PE2I as an imaging tool of the nigrostriatal pathway.

255 r deafferentation of the corticostriatal and nigrostriatal pathways may mitigate striatal stress and

256 hippocampus and basal ganglia (specifically nigrostriatal pathways).

257 chemical lesions of the corticostriatal and nigrostriatal pathways, respectively, improved the behav

258 Effects on nigrostriatal-projecting neurons were examined using a r

259 living animal models of degeneration in the nigrostriatal projection that a constitutively active fo

260 lude that regrowth of axons within the adult nigrostriatal projection, a system that is prominently a

261 Mesoaccumbal and nigrostriatal projections are sensitive to stress, and h

262 through altered afferent corticostriatal and nigrostriatal projections that may modulate synaptically

263 ial inflammatory responses and led to robust nigrostriatal protection.

264 ations in rats with unilateral lesion in the nigrostriatal region induced by neurotoxin 6-OHDA, a Par

265 ) treatment in vivo, Nur77 expression in the nigrostriatal region is dramatically reduced.

266 rons and defective dopamine signaling in the nigrostriatal region.

267 The distribution volume reduction across nigrostriatal regions at 8 weeks ranged from 13-16%, wit

268 abundantly expressed in non-DA cells in the nigrostriatal regions.

269 ical benefit mediated by graft survival with nigrostriatal reinnervation.

270 emonstrate that STN DBS does not protect the nigrostriatal system against alpha-syn overexpression-me

271 Degeneration of the dopaminergic nigrostriatal system and of noradrenergic neurons in the

272 ) dopamine neurons and increases BDNF in the nigrostriatal system and primary motor cortex.

273 ntified as a factor that plays a role in the nigrostriatal system during development and in response

274 that prediction error signals in the brain's nigrostriatal system guide learning for trial-and-error

275 ed cortical impact (CCI) injury on TH in the nigrostriatal system is currently unknown.

276 We speculate that the increase in TH in the nigrostriatal system may reflect a compensatory response

277 aterally increased at 28 days post-injury in nigrostriatal system revealed by immunohistochemistry in

278 neurons induces remarkable adaptions in the nigrostriatal system where limited amounts of dopamine i

279 In the nigrostriatal system, BDNF expression was upregulated in

280 e played by the tVTA as a GABA brake for the nigrostriatal system, demonstrating a critical influence

281 he result of dopaminergic dysfunction of the nigrostriatal system, the clinical manifestations of Par

282 paminergic glutathione levels in vivo on the nigrostriatal system, we created genetically engineered

283 function of TGF-beta signaling in the adult nigrostriatal system, we generated transgenic mice with

284 lated motor deficits and degeneration of the nigrostriatal system.

285 rescued with ectopic Nur77 expression in the nigrostriatal system.

286 he loss of dopamine-producing neurons in the nigrostriatal system.

287 role in protection and reconstruction of the nigrostriatal system.

288 ioned) compared with the noninjured (saline) nigrostriatal system.

289 nigra (SN) and affected the integrity of the nigrostriatal system.

290 ntially regulates trophic factors within the nigrostriatal system.

291 ophic factors in the intact and degenerating nigrostriatal system.

292 on and separate parsing of inputs within the nigrostriatal system.SIGNIFICANCE STATEMENT Prior studie

293 of rates of metabolism in the mesolimbic and nigrostriatal systems with the amount of MPD-induced beh

294 ut only correlates with in vitro measures of nigrostriatal terminal fields when nigral cell loss does

295 urons in substantia nigra or degeneration of nigrostriatal terminals at 12 months.

296 OPA and NET-mediated DA reuptake in lesioned nigrostriatal terminals may have a role in LID severity

297 vation of presynaptic nicotinic receptors on nigrostriatal terminals that evoke GABA release from the

298 anine (S129A) or to aspartate (S129D) in the nigrostriatal tract of the rat to investigate the effect

299 mmunoreactive neurons and total cells in the nigrostriatal tract, improves the motor performance in M

300 s, proving a regulatory role of FGF-2 during nigrostriatal wiring.