ライフサイエンスコーパス: substantia nigra

1 men, nucleus accumbens, globus pallidus, and substantia nigra).

2 ing KORD to midbrain (ventral tegmental area/substantia nigra).

3 mpared with healthy controls, but not in the substantia nigra.

4 pigmented dopaminergic neuronal count in the substantia nigra.

5 ed connectivity between ventral striatum and substantia nigra.

6 imarily in the dopaminergic neurons of human substantia nigra.

7 after lesioning dopaminergic neurons of the substantia nigra.

8 uclear palsy have elevated free-water in the substantia nigra.

9 owed by death of dopaminergic neurons in the substantia nigra.

10 elective loss of dopaminergic neurons in the substantia nigra.

11 parkinsonism had elevated free-water in the substantia nigra.

12 was measured in dopaminergic cells from the substantia nigra.

13 y of AAV2-neurturin delivered to putamen and substantia nigra.

14 xonal transport of neurturin from putamen to substantia nigra.

15 ffects on residual dopaminergic cells in the substantia nigra.

16 tors expressing human alpha-synuclein in the substantia nigra.

17 ntial non-invasive progression marker of the substantia nigra.

18 d by the loss of dopaminergic neurons in the substantia nigra.

19 d-drawn regions of interest in the posterior substantia nigra.

20 ps in the thalamic reticular nucleus and the substantia nigra.

21 ependent currents in dopamine neurons in the substantia nigra.

22 ucleus (STN), globus pallidus, striatum, and substantia nigra.

23 gressive loss of dopaminergic neurons in the substantia nigra.

24 induced loss of dopaminergic neurons in the substantia nigra.

25 yrosine hydroxylase-immunostained neurons in substantia nigra.

26 d by the loss of dopaminergic neurons in the substantia nigra.

27 essive loss of dopaminergic neurons from the substantia nigra.

28 degeneration of dopaminergic neurons in the substantia nigra.

29 bellar systems and dopaminergic cells of the substantia nigra.

30 ed numbers of activated myeloid cells in the substantia nigra.

31 c model, the SVPE signal was detected in the substantia nigra.

32 yrosine hydroxylase (TH)-positive neurons of substantia nigra.

33 RD3-rich regions of the ventral pallidum and substantia nigra.

34 d by the loss of dopaminergic neurons in the substantia nigra.

35 sencephalic dopaminergic (DA) neurons in the substantia nigra.

36 lidus but decrease in entopeduncular nucleus/substantia nigra.

37 elective loss of dopaminergic neurons of the substantia nigra.

38 sterior thalamus (0.26% increase, P < .001), substantia nigra (0.25% increase, P = .01), red nucleus

39 lthough a trend in BP(ND) was present in the substantia nigra (-14% +/- 15%).

40 y was low in the pallidum (6%) but higher in substantia nigra (19%), thalamus (14%), and hypothalamus

41 AAV2-neurturin injected bilaterally into the substantia nigra (2.0 x 10(11) vector genomes) and putam

42 d better survival of dopaminergic neurons in substantia nigra and an increased number of microglia ex

43 tmortem samples that human catecholaminergic substantia nigra and locus coeruleus neurons express MHC

44 tum and the catecholaminergic neurons of the substantia nigra and locus coeruleus, which are implicat

45 Depigmentation of the substantia nigra and other brainstem nuclei was present.

46 duced density of dopaminergic neurons in the substantia nigra and reduced dopaminergic fibres in the

47 e changes to PDE10A in striatoentopeduncular/substantia nigra and striatopallidal pathways might tigh

48 ualized directly by two-photon microscopy in substantia nigra and striatum brain slices.

49 l, parietal and temporal cortices, striatum, substantia nigra and subthalamic nucleus were assessed.

50 olve the loss of dopaminergic neurons in the substantia nigra and the coincidental appearance of Lewy

51 d by the loss of dopaminergic neurons in the substantia nigra and the formation of Lewy body inclusio

52 oss of dopaminergic (DAergic) neurons in the substantia nigra and the gradual depletion of dopamine (

53 , including dopaminergic deficiencies in the substantia nigra and the premotor and motor cortices, an

54 d by the loss of dopaminergic neurons in the substantia nigra and the presence of intraneuronal inclu

55 their projections to entopeduncular nucleus/substantia nigra and to external globus pallidus.

56 ctedly, this effect was not reflected in the substantia nigra and ventral tegmental area (SN/VTA), me

57 BPND in a midbrain region, encompassing the substantia nigra and ventral tegmental area, in 18 daily

58 as extensive dopaminergic neuron loss in the substantia nigra and widespread classic Lewy body pathol

59 our, 2.64; 95% CI, 1.40-4.99; Lewy bodies in substantia nigra and/or locus ceruleus in ACT: RR for TB

60 tyrosine hydroxylase-positive neurons in the substantia nigra, and attenuated the decrease of striata

61 audate, anterior putamen, posterior putamen, substantia nigra, and nucleus accumbens were significant

62 the same cortical areas via globus pallidus, substantia nigra, and thalamus.

63 d on GABAergic neurons of the basal ganglia, substantia nigra, and ventral tegmental area (VTA) where

64 The striatum as well as substantia nigra appeared normal and no loss of dopamine

65 h neuronal iron and nitric oxide (NO) in the substantia nigra are associated with Parkinson's disease

66 Dopamine midbrain neurons within the substantia nigra are particularly prone to degeneration

67 was to validate free water in the posterior substantia nigra as a progression marker in Parkinson's

68 AAV2-neurturin delivery to the putamen and substantia nigra bilaterally in PD was not superior to s

69 Beyond the substantia nigra, both multiple system atrophy and progr

70 ly effective contacts included the thalamus, substantia nigra, brainstem and superior frontal gyrus.

71 ypical disease-associated regions (striatum, substantia nigra), but also within anterior cingulate co

72 endogenous alpha-synuclein in the adult rat substantia nigra by adeno-associated virus-mediated deli

73 positive Lewy bodies and neurites and severe substantia nigra cell loss.

74 ubiquitin chains and markedly reduced in the substantia nigra compared with the neocortex.

75 ytes and two brain regions, the amygdala and substantia-nigra, compared to controls.

76 imity to a presumed disease epicenter in the substantia nigra, compatible with a trans-neuronal sprea

77 rized by the loss of dopamine neurons in the substantia nigra, decreased striatal dopamine levels, an

78 Furthermore, we detected elevated substantia nigra dopamine messenger RNA levels of NCS-1

79 provides a novel promising target for tuning substantia nigra dopamine neuron activity, and their vul

80 Substantia nigra dopamine neurons are involved in behavi

81 Substantia nigra dopamine neurons fire tonically resulti

82 ysiological recordings in brain slices, that substantia nigra dopamine neurons from mice 25-30 months

83 firing of action potentials could predispose substantia nigra dopamine neurons to selective neurodege

84 in slice multiphoton microscopy to show that substantia nigra dopamine neurons, which are sensitive t

85 ysosomal dysfunction have been implicated in substantia nigra dopaminergic neurodegeneration in Parki

86 20N VPS35 induces the marked degeneration of substantia nigra dopaminergic neurons and axonal patholo

87 f dopamine inhibition.SIGNIFICANCE STATEMENT Substantia nigra dopaminergic neurons can be divided int

88 to characterize the postnatal development of substantia nigra dopaminergic neurons' electrical phenot

89 ha-synuclein aggregation and degeneration of substantia nigra dopaminergic neurons.

90 circuits, and may provide a means to inhibit substantia nigra dopaminergic neurons.

91 S inhibited key brain regions, including the substantia nigra, entopeduncular nucleus, and nucleus ac

92 usly found elevated free-water levels in the substantia nigra for patients with Parkinson's disease c

93 ohistochemical analysis of human post-mortem substantia nigra from Parkinson's disease suggests that

94 However, neurons of the substantia nigra from the LND cases showed reduced melan

95 There were group differences in the substantia nigra, globus pallidus, pulvinar thalamus, th

96 e over 1 year in free water in the posterior substantia nigra in a large cohort of de novo patients w

97 nesis and protects mature neurons within the substantia nigra in a mouse model of Parkinson's disease

98 levels in the D-loop region is found in the substantia nigra in Parkinson disease (n = 10) with resp

99 lterations in other brain regions beyond the substantia nigra in Parkinson's disease, multiple system

100 ynthase (iNOS)-positive myeloid cells in the substantia nigra in response to alpha-synuclein overexpr

101 Moreover, overexpression of necdin in the substantia nigra in vivo of adult mice protects dopamine

102 that: (i) free water level in the posterior substantia nigra increased over 1 year in de novo Parkin

103 ted by RO5166017 when microinjected into the substantia nigra, infralimbic cortex, BLA, and CeA.

104 demonstrate that free water in the posterior substantia nigra is a valid, progression imaging marker

105 Free-water in the posterior substantia nigra is elevated in Parkinson's disease, inc

106 ent and in-depth characterization from human substantia nigra is necessary.

107 ch as rotarod and treadmill tests, caused by substantia nigra lesioning in mice.

108 tor traits and postmortem indices, including substantia nigra Lewy bodies and neuronal loss.

109 nucleus (n = 13), globus pallidus (n = 13), substantia nigra (n = 13), posterior thalamus (n = 12),

110 death in cultured neurons in vitro, in mouse substantia nigra neurons in vivo and in human fibroblast

111 Similarly, TRPC1(-/-) substantia nigra neurons showed increased L-type Ca(2+)

112 neration of dopaminergic (DA) neurons in the substantia nigra, non-motor symptoms including anxiety,

113 Direct measures of DNAm in the substantia nigra of 39 cases and 13 control samples were

114 erexpression of human alpha-synuclein in the substantia nigra of aged (18 to 21-month-old) L444P Gba1

115 he midbrain of macaque monkeys, close to the substantia nigra of both sides.

116 d non-CpG sites in the entorhinal cortex and substantia nigra of control human postmortem brains, usi

117 wild-type and mutant alpha-synuclein in the substantia nigra of mice demonstrated that blocking alph

118 erely reduced in dopaminergic neurons of the substantia nigra of Parkinson's disease (PD) patients an

119 were found to be increased in the posterior substantia nigra of Parkinson's disease compared with co

120 the hypotheses that free-water levels in the substantia nigra of Parkinson's disease increase followi

121 s models have provided mixed findings in the substantia nigra of Parkinson's disease, but recent work

122 was increased in the anterior and posterior substantia nigra of Parkinson's disease, multiple system

123 longitudinally over 1 year in the posterior substantia nigra of Parkinson's disease.

124 reflect the loss of pigmented neurons in the substantia nigra of parkinsonian patients.

125 water values were increased in the posterior substantia nigra of patients with Parkinson's disease co

126 hat RGMa is significantly upregulated in the substantia nigra of patients with Parkinson's disease.

127 ed with aggregated synuclein deposits in the substantia nigra of patients with Parkinson's disease.

128 complex I activity have been observed in the substantia nigra of PD patients, and loss of Parkin resu

129 lecule member a (RGMa) is upregulated in the substantia nigra of PD patients.

130 tyrosine hydroxylase-positive neurons in the substantia nigra of PLP-SYN mice.

131 When injected into the substantia nigra of rat brains, DOPAL causes the loss of

132 nd neurological diseases are enhanced in the substantia nigra of rats with alpha-SYN overexpression,

133 ate alpha-synuclein toxicity in vivo, in the substantia nigra of rats.

134 ates in the cortex, hippocampus, stratum and substantia nigra of the nGD mice.

135 ) and neuromelanin-containing neurons in the substantia nigra (off-target binding).

136 t anatomic regions of involvement (striatum, substantia nigra, olivary and pontine nuclei, hippocampu

137 absence of a swallow-tail appearance in the substantia nigra on high-resolution SWI, representing ni

138 ficantly decrease BPND in the putamen or the substantia nigra or in any region when measured with [(1

139 ntially expressed in striatoentopeducuncular/substantia nigra or striatopallidal pathways, respective

140 onation and subsequently inoculated into the substantia nigra or striatum of wild-type mice and macaq

141 increases in R2* occur during 2 years in the substantia nigra (P < .001) and globus pallidus (P = .03

142 ne hydroxylase immunoreactive neurons in the substantia nigra (p<0.05).

143 related to Parkinson's disease (PD), in the substantia nigra par compacta (SNpc) of the brain in a P

144 neurons and dopaminergic neurons in the rat substantia nigra pars compact, increases the recruitment

145 Dopamine neurons from the substantia nigra pars compacta (SNc) and ventral tegment

146 The rodent ventral tegmental area (VTA) and substantia nigra pars compacta (SNC) contain dopamine ne

147 Substantia nigra pars compacta (SNc) dopamine neurons an

148 TATEMENT Prior studies have established that substantia nigra pars compacta (SNc) dopamine neurons ar

149 to be a major factor underlying the loss of substantia nigra pars compacta (SNc) dopaminergic neuron

150 Burst spiking in substantia nigra pars compacta (SNc) dopaminergic neuron

151 on and behavior that depend on the firing of substantia nigra pars compacta (SNc) dopaminergic neuron

152 tion of a region homologous to the mammalian substantia nigra pars compacta (SNc) evokes increasing a

153 tanding how dopaminergic (DA) neurons of the substantia nigra pars compacta (SNc) govern movements re

154 date the role of this receptor in regulating substantia nigra pars compacta (SNc) neuron physiology i

155 regarding functional heterogeneity among the substantia nigra pars compacta (SNc) neurons.

156 nalling pathways and have been implicated in substantia nigra pars compacta (SNc) pathology in Parkin

157 s unclear to what extent dopamine neurons in substantia nigra pars compacta (SNc) play such roles.

158 The substantia nigra pars compacta (SNc) projects specifical

159 c dopaminergic (mdDA) neurons, including the substantia nigra pars compacta (SNc) subpopulation that

160 ered a type of dopamine neuron in the monkey substantia nigra pars compacta (SNc) that retains past l

161 tVTA on the nigrostriatal pathway, from the substantia nigra pars compacta (SNc) to the dorsal stria

162 Most dopaminergic neurons in the substantia nigra pars compacta (SNc), but not in ventral

163 It has been suggested that, in the substantia nigra pars compacta (SNc), the pacemaking rel

164 ic inputs and project to dopamine neurons in substantia nigra pars compacta (SNc), whereas matrix neu

165 the diversity of dopamine neurons within the substantia nigra pars compacta (SNc).

166 degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc).

167 specifically in dopaminergic neurons of the substantia nigra pars compacta (SNc).

168 erents from ventral tegmental area (VTA) and substantia nigra pars compacta (SNc).

169 and dendrites of dopamine neurons within the substantia nigra pars compacta (SNc).

170 the tuberculum posterior, a homologue of the substantia nigra pars compacta (SNc)/ventral tegmental a

171 TN DBS) protects dopaminergic neurons of the substantia nigra pars compacta (SNpc) against 6-OHDA and

172 Loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) and of noradrenerg

173 ic connections onto these neurons in the rat substantia nigra pars compacta (SNpc) and ventral tegmen

174 acterized by loss of dopamine neurons in the substantia nigra pars compacta (SNpc) and widespread agg

175 n travel to higher centers, compromising the substantia nigra pars compacta (SNpc) and, later, the ce

176 oxylase-immunoreactive (THir) neurons in the substantia nigra pars compacta (SNpc) compared with sali

177 ions of dopaminergic (DA) neurons within the substantia nigra pars compacta (SNpc) display a differen

178 rential dysfunction/degeneration of midbrain substantia nigra pars compacta (SNpc) dopaminergic (DA)

179 g is elevated in dopaminergic neurons of the substantia nigra pars compacta (SNpc) of human PD patien

180 ive dopaminergic (DA) neurons at the ventral substantia nigra pars compacta (SNpc) preferentially deg

181 significant loss of dopaminergic neurons in substantia nigra pars compacta (SNpc), and there was no

182 featuring progressive degeneration of DNs in substantia nigra pars compacta (SNpc), decreased striata

183 euromelanin signal intensity loss within the substantia nigra pars compacta (SNpc), locus coeruleus,

184 ucleolar volume of dopaminergic cells in the substantia nigra pars compacta (SNpc), ventral tegmental

185 elective loss of dopaminergic neurons of the substantia nigra pars compacta (SNpc).

186 to PPN cholinergic terminals in the ventral substantia nigra pars compacta (vSNc) or to the ventral

187 ressive loss of dopaminergic (DA) neurons in substantia nigra pars compacta and age-dependent L-DOPA-

188 he activity of dopaminergic neurons from the substantia nigra pars compacta and noradrenergic neurons

189 volved in T cell trafficking, in vivo in the substantia nigra pars compacta and the serum of 1-methyl

190 diencephalic dopamine neurons located in the substantia nigra pars compacta and the ventral tegmental

191 Midbrain dopaminergic (DA) neurons in the substantia nigra pars compacta and ventral tegmental are

192 Dopamine neurons in the substantia nigra pars compacta and ventral tegmental are

193 ured by reduced dopamine terminal damage and substantia nigra pars compacta cell loss.

194 ake stronger projections to the striatum and substantia nigra pars compacta compared with PV-GPe neur

195 n addition, in vivo recordings of identified substantia nigra pars compacta dopamine neurons in R1441

196 rial integrity and thereby properly maintain substantia nigra pars compacta dopaminergic neurons and

197 Studying mouse substantia nigra pars compacta dopaminergic neurons both

198 reas selective degeneration of DA neurons in substantia nigra pars compacta is a key neuropathologica

199 degeneration of dopaminergic neurons in the substantia nigra pars compacta is the primary cause for

200 ptor kinase type B (trkB) receptor occurs in substantia nigra pars compacta neurons and is required f

201 sed within vulnerable dopaminergic (DAergic) substantia nigra pars compacta neurons, only select down

202 ES and eotaxin were also up-regulated in the substantia nigra pars compacta of post-mortem PD brains

203 degeneration of dopaminergic neurons in the substantia nigra pars compacta portion of the brain.

204 rabrachial pigmented nucleus and dorsomedial substantia nigra pars compacta) mesodiencephalic dopamin

205 the degeneration of dopamine neurons of the substantia nigra pars compacta, a deficit in dopamine ne

206 d neurons and in dopaminergic neurons of the substantia nigra pars compacta, a susceptible brain regi

207 or abnormal protein accumulation within the substantia nigra pars compacta, suggesting that nigrostr

208 heterogeneous subgroups of neurons, such as substantia nigra pars compacta, ventral tegmental area a

209 idal neurons and dopaminergic neurons of the substantia nigra pars compacta.

210 hanism within the ventral tegmental area and substantia nigra pars compacta.

211 preferential loss of dopamine neurons in the substantia nigra pars compacta.

212 striatum and dopamine neuron activity in the substantia nigra pars compacta.

213 action potentials in dopamine neurons of the substantia nigra pars compacta.

214 ially innervated dopaminergic neurons in the substantia nigra pars compacta.

215 tely dissociated dopamine neurons from mouse substantia nigra pars compacta.

216 ne (6-OHDA) in the dorsal GL or in the right substantia nigra pars compacta.

217 as striatal cholinergic interneurons and the substantia nigra pars compacta.

218 show high levels of LRRK2 expression in the substantia nigra pars compacta.

219 (SNc), but not in ventral tegmental area or substantia nigra pars lateralis, consistently represente

220 rvated the caudal-dorsal-lateral part of the substantia nigra pars reticulata (cdlSNr), directly or i

221 n the 25-40 Hz range in LFPs recorded in the substantia nigra pars reticulata (SNpr) and motor cortex

222 ons from the pedunculopontine nucleus to the substantia nigra pars reticulata (SNr) act on muscarinic

223 taneous firing of GABAergic neurons in mouse substantia nigra pars reticulata (SNr) brain slices.

224 the output of the basal ganglia through the substantia nigra pars reticulata (SNr) controls active a

225 vo recording, we measured BG output from the substantia nigra pars reticulata (SNr) in mice while mon

226 pontaneously active GABAergic neurons of the substantia nigra pars reticulata (SNr), a major output o

227 observed to reach their midbrain target, the substantia nigra pars reticulata (SNr), at E14 in the mo

228 We recorded from the substantia nigra pars reticulata (SNR), the major basal

229 a both the ipsilateral and the contralateral substantia nigra pars reticulata (SNr).

230 eliminate, glutamatergic transmission in the substantia nigra pars reticulata and entopeduncular nucl

231 rojection neurons in the dorsal striatum and substantia nigra pars reticulata by activating TRPM2 cha

232 activity measured in the globus pallidus and substantia nigra pars reticulata is caused by abnormal s

233 keeping constant the average firing rate of substantia nigra pars reticulata reduces the incidence o

234 r, the GABAergic output projections from the substantia nigra pars reticulata to the deep layers of t

235 We found that activity in the substantia nigra pars reticulata, a basal ganglia output

236 entially innervated GABAergic neurons in the substantia nigra pars reticulata.

237 , and that baseline free-water levels in the substantia nigra predict the change in bradykinesia foll

238 year increase in free water in the posterior substantia nigra predicts subsequent long-term progressi

239 riatal projections to entopeduncular nucleus/substantia nigra, preferentially expressing D1 receptors

240 lear need to develop non-invasive markers of substantia nigra progression in Parkinson's disease.

241 e show that feedback via axon collaterals of substantia nigra projection neurons control the gain of

242 Substantia nigra, putamen, and cortical p11 protein leve

243 d images was seen in the posterior thalamus, substantia nigra, red nucleus, cerebellar peduncle, coll

244 MTA1, we analyzed MTA1 and TH levels in the substantia nigra region of a large cohort of human brain

245 rhythmic activity of adult DA neurons in the substantia nigra region.

246 me studies of neuromelanin granules in human substantia nigra required high tissue amounts.

247 ny neurons (MSNs) directly projecting to the substantia nigra reticulata (SNr) lose tonic presynaptic

248 OFQ functionally opposes DOP transmission in substantia nigra reticulata and that NOP receptor antago

249 y, immunohistochemistry analysis for MTA1 in substantia nigra sections revealed that 74.1% of the sam

250 ers to demonstrate that the VTA, but not the substantia nigra, sends dense intra- and interhemispheri

251 degeneration of dopaminergic neurons in the substantia nigra (SN) and affected the integrity of the

252 (PD), including dopaminergic neurons of the substantia nigra (SN) and cholinergic neurons of the dor

253 ndent dopaminergic (DA) neuronal loss in the substantia nigra (SN) and ventral tegmental area (VTA),

254 The substantia nigra (SN) consists of GABAergic neurons of t

255 tokine production leading to degeneration of substantia nigra (SN) dopamine (DA) neurons, mimicking i

256 models, STN DBS provides neuroprotection for substantia nigra (SN) dopamine neurons and increases BDN

257 CR attenuated the MPTP-induced loss of substantia nigra (SN) dopamine neurons and striatal dopa

258 Animal studies have shown that substantia nigra (SN) dopaminergic (DA) neurons strength

259 ized pathologically by the selective loss of substantia nigra (SN) dopaminergic (DAergic) neurons.

260 rons in the ventral tegmental area (VTA) and substantia nigra (SN) has been examined at multiple leve

261 The dopaminergic substantia nigra (SN) is implicated in the drive to expl

262 tial loss of highly vulnerable dopamine (DA) substantia nigra (SN) neurons.

263 Dopaminergic neurons of the substantia nigra (SN) play a vital role in everyday task

264 DA neurons originating in the substantia nigra (SN) projecting to the dorsal striatum

265 The substantia nigra (SN) provides the largest dopaminergic

266 ulnerability of dopamine (DA) neurons in the substantia nigra (SN) to neurodegenerative stressors cau

267 cal and functional organization of the human substantia nigra (SN) using diffusion and functional MRI

268 for the caudate, putamen, ventral striatum, substantia nigra (SN), and cerebellum were manually draw

269 ain, e.g., the subventricular zone (SVZ) and substantia nigra (SN), have promising potential to repla

270 ng human alpha-syn fibril seeds into the rat substantia nigra (SN), in combination with adenoassociat

271 ventral tegmental area (VTA), but not in the substantia nigra (SN), of D2R-OE mice.

272 rest (ROIs): the dentate nucleus (DN), pons, substantia nigra (SN), pulvinar thalami, and globus pall

273 vels within dopaminergic (DA) neurons in the substantia nigra (SN), which may contribute to their sel

274 Rats were injected unilaterally, in the substantia nigra (SN), with AAV1/2-A53T-aSyn or control

275 al tegmental area (VTA) and the other in the substantia nigra (SN).

276 pamine transporter (DAT) in the striatum and substantia nigra (SN).

277 gation of alpha-synuclein (alpha-syn) in the substantia-nigra (SN).

278 Iron concentrations were assessed in the substantia nigra (SNc), dentate and caudate nucleus, red

279 associated with increased iron levels in the substantia nigra (SNc).

280 or colliculus through different parts of the substantia nigra so that the animal looks preferentially

281 afferents to the ventral tegmental area and substantia nigra; the dopamine systems themselves; gluta

282 Increasing TGF-beta signaling in the substantia nigra through adeno-associated virus expressi

283 turally similar to those isolated from human substantia nigra tissues.

284 caused by a loss of dopamine input from the substantia nigra to the striatum.

285 ortem by the loss of dopamine neurons in the substantia nigra together with the presence of Lewy bodi

286 minescence imaging in the mouse striatum and substantia nigra up to 8 months after injection.

287 dorsal STN (mood, anxiety), and inferior STN/substantia nigra (UPDRS tremor, working memory).

288 that, in contrast to dopamine neurons in the substantia nigra, vagal motoneurons do not enhance their

289 a large number of CARTp-ir terminals in the substantia nigra, ventral tegmental area, periaqueductal

290 igher tracer binding in D3-rich regions: the substantia nigra/ventral tegmental area (SN/VTA) (+20%;

291 adaptive coding, BOLD response slopes in the Substantia Nigra/Ventral Tegmental Area (SN/VTA) and ven

292 s effect depends on interactions between the substantia nigra/ventral tegmental area complex (SN/VTA)

293 ased by 45% and the mean total (18)F-AV-1451 substantia nigra volume of distribution was decreased by

294 response to value in ventral tegmental area/substantia nigra (VTA/SN) shows context-sensitivity, an

295 vival of tyrosine hydroxylase neurons in the substantia nigra was determined by stereological tests a

296 Neuronal loss of the substantia nigra was either absent or very mild in the p

297 emonstrated that free water in the posterior substantia nigra was elevated in Parkinson's disease com

298 The bilateral substantia nigra was evaluated by two neuroradiologists

299 type 2 density for the caudate, putamen,and substantia nigra were 21.50%, 58.20%, and 21.10% for mil

300 n after lipopolysaccharide injections in the substantia nigra, with a marked increase in the recruitm