ライフサイエンスコーパス: substantia nigra

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

2 gnaling, and loss of dopamine neurons in the substantia nigra.

3 ain, encompassing ventral tegmental area and substantia nigra.

4 egions to dopamine-containing neurons of the substantia nigra.

5 rder involving dopaminergic neurons from the substantia nigra.

6 ropagation from the most likely seed region, substantia nigra.

7 heral blood, frontal cortex, cerebellum, and substantia nigra.

8 including the caudate-putamen, striatum and substantia nigra.

9 of dopamine from both ventral tegmentum and substantia nigra.

10 ted with selective D-serine reduction in the substantia nigra.

11 orm gyrus, amygdala, striatum, pulvinar, and substantia nigra.

12 to the loss of dopaminergic neurons from the substantia nigra.

13 irectly (dMSNs) or indirectly (iMSNs) to the substantia nigra.

14 elective loss of dopaminergic neurons in the substantia nigra.

15 was measured in dopaminergic cells from the substantia nigra.

16 degeneration of dopaminergic neurons in the substantia nigra.

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

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

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

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

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

22 lidus but decrease in entopeduncular nucleus/substantia nigra.

23 elective loss of dopaminergic neurons of the substantia nigra.

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

25 pigmented dopaminergic neuronal count in the substantia nigra.

26 ed connectivity between ventral striatum and substantia nigra.

27 imarily in the dopaminergic neurons of human substantia nigra.

28 after lesioning dopaminergic neurons of the substantia nigra.

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

30 of the basal Iba1-positive population in the substantia nigra.

31 rmined using a voxelwise analysis within the substantia nigra.

32 es were localized in distinct regions of the substantia nigra.

33 ources controls neuronal migrations into the substantia nigra.

34 ha-synuclein aggregates into the striatum or substantia nigra.

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

36 acterized by loss of dopamine neurons in the substantia nigra(1).

37 oradiography, we confirmed lower SV2A in the substantia nigra (-17%; p < 0.005) and nonsignificant fi

38 ding potentials in the caudate, putamen, and substantia nigra (4.9, 4.9, and 1, respectively) were si

39 on disease group exhibited lower SV2A in the substantia nigra (-45%; p < 0.001), red nucleus (-31%; p

40 hosphorylated alpha-synuclein in ipsilateral substantia nigra and adjacent to the injection site.

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

42 oss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation

43 degeneration of dopaminergic neurons in the substantia nigra and cholinergic neurons in the dorsal m

44 EAT1 is overexpressed in Parkinson's disease substantia nigra and confers drug-inducible neuroprotect

45 e the gene-gene regulatory structures in the substantia nigra and determine key regulators of the PD

46 DNER is highly expressed in substantia nigra and is an activator of the NOTCH1 pathw

47 ns in brain were between ADGRV1 and GRIK2 in substantia nigra and medullary inferior olivary nucleus,

48 (n = 15) and normal controls (n = 13) in the substantia nigra and putamen.

49 ngs using post-mortem histology of the human substantia nigra and radiotracer studies of the human st

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

51 s that originates at least from two sources, substantia nigra and thalamic reticular nucleus.

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

53 her groups, and in globus pallidus, putamen, substantia nigra and the dentate nucleus compared to PD

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

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

56 in neuromelanin-sensitive MRI signal in the substantia nigra and their relation to clinical scores o

57 art in the posterolateral motor areas of the substantia nigra and then progressed to more medial area

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

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

60 l dopamine-rich midbrain nuclei, such as the substantia nigra and ventral tegmental area, also exhibi

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

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

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

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

65 l when isolated from postmortem PD patients' substantia nigra; and (b) leucine-rich repeat kinase 2 (

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

67 M-MRI signal in ventrolateral regions of the substantia nigra (area under the receiver operating char

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

69 ore abundant in globus pallidus internus and substantia nigra at 6 months and remained so at 18 month

70 f subcortical structures including striatum, substantia nigra, basal forebrain (BF), pedunculopontine

71 s post-surgery), and to the putamen plus the substantia nigra bilaterally in the second (8 years post

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

73 ncluded the ethmoid sinus, clivus, meninges, substantia nigra, but not the basal ganglia or choroid p

74 Degeneration of dopaminergic neurons in the substantia nigra causes the motor symptoms of Parkinson'

75 ns project to the ventral tegmental area and substantia nigra compacta but Nts(Dehy) neurons do not.

76 Second, we analyzed expression in the human substantia nigra, comparing cell states in specific dono

77 numerous cells of the ventral tegmental area/substantia nigra complex.

78 mitter in the striatum, while only few adult substantia nigra DA neurons have this capacity.

79 Moreover, direct stimulation of VTA or substantia nigra dopamine cell bodies failed to induce f

80 creased ventral tegmental area and decreased substantia nigra dopamine neuron population activity.

81 Substantia nigra dopamine neurons have been implicated i

82 otoxicity, as shown by increased survival of substantia nigra dopamine neurons, integrity of striatal

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

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

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

86 19S LRRK2 induces the robust degeneration of substantia nigra dopaminergic neurons, a pathological ha

87 TAAR1 prevents glutamate accumulation in the substantia nigra during hyperlocomotive states.

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

89 mic and transcriptomic data from putamen and substantia nigra from 117 human brains, interrogating re

90 Volumetric measurement of hyperintense substantia nigra from magnetization transfer-prepared T1

91 n particular the ictal increase in firing of substantia nigra GABAergic neurons.

92 ollowing the loss of dopamine neurons in the substantia nigra has been known for the last 50.

93 er-prepared T1-weighted MRI volumetry of the substantia nigra helped differentiate the stages of Park

94 Substantia nigra hyperechogenicity, olfactory loss, depr

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

96 ir axons to the targeted globus pallidus and substantia nigra in a time-dependent manner.

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

98 The ratio between the volume of the substantia nigra in patients with Parkinson's disease re

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

100 nd tyramine reduced glutamate release in the substantia nigra in wild-type but not in TAAR1-KO mice.

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

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

103 the anatomical and functional subdivision of substantia nigra into dorsal and ventral tiers and stria

104 I can depict a hyperintense subregion of the substantia nigra involved in the degeneration process of

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

106 y, netrin-1 is highly expressed in the adult substantia nigra, leading us to investigate a role of th

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

108 ritability of Parkinson's disease within the substantia nigra module.

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

110 mentary refers to 'Spatiotemporal changes in substantia nigra neuromelanin content in Parkinson's dis

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

112 In the substantia nigra, neurturin expression was detected in 9

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 we show that silencing netrin-1 in the adult substantia nigra of mice induces DCC cleavage and a sign

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

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

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

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

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

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

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

127 romelanin-containing dopaminergic neurons in substantia nigra of PD patients.

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

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

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

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

132 (mDA) or cortical glutamate neurons into the substantia nigra or striatum of a mouse PD model and fou

133 attenuate the activation of microglia in the substantia nigra par compacta of MPTP-treated mice.

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

135 eurons migrate to form the laterally-located substantia nigra pars compacta (SN) and medially-located

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

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

138 Dopaminergic neurons (DAs) of the rodent substantia nigra pars compacta (SNc) display varied elec

139 e neurodegenerative disease characterized by substantia nigra pars compacta (SNc) dopamine (DA) neuro

140 Substantia nigra pars compacta (SNc) dopamine neurons an

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

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

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

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

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

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

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

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

149 ion between ventral tegmental area (VTA) and substantia nigra pars compacta (SNc), no clear evidence

150 ration of dopaminergic neurons (DaNs) of the substantia nigra pars compacta (SNc), resulting in the c

151 arkinson disease (PD)-related changes in the substantia nigra pars compacta (SNc), the key pathologic

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

153 significant loss of dopamine neurons in the substantia nigra pars compacta (SNc).

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

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

156 ressive loss of dopamine (DA) neurons in the substantia nigra pars compacta (SNc).

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

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

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

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

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

162 Neuronal loss in the substantia nigra pars compacta (SNpc) in Parkinson disea

163 Here we show that optogenetic activation of substantia nigra pars compacta (SNpc) neurons alleviates

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

165 tion of the dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) remains to be answ

166 ng activity, reduced dopaminergic neurons in substantia nigra pars compacta (SNpc), and SNCA mice wer

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

168 , loss of dopaminergic neurons (DANs) in the substantia nigra pars compacta (SNpc), decrease of dopam

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

170 n neuromelanin-containing cell levels in the substantia nigra pars compacta and nigrostriatal termina

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

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

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

174 e the interpeduncular nucleus, raphe nuclei, substantia nigra pars compacta and ventral tegmental are

175 Inhibiting both ventral tegmental area and substantia nigra pars compacta DA neurons in the post-re

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

177 AIS length or distance from the soma in rat substantia nigra pars compacta dopaminergic neurons.

178 ted overexpression of alpha-synuclein in the substantia nigra pars compacta impacts visual processing

179 Degeneration of nigrostriatal neurons of substantia nigra pars compacta in Parkinson's disease re

180 c fibres from the ventral tegmental area and substantia nigra pars compacta innervate the majority of

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

182 insight into how neuron subtypes outside the substantia nigra pars compacta may be compensating at a

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

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

185 In vivo data from the cortex and substantia nigra pars compacta of aged LRRK2 transgenic

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

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

188 iched brain fraction from frontal cortex and substantia nigra pars compacta tissue, isolated by sever

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

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

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

192 ally severe neuronal loss and gliosis in the substantia nigra pars compacta, without Lewy bodies.

193 eral amygdala, dorsal raphe nucleus, and the substantia nigra pars compacta.

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

195 d-phenylalanine was infused locally into the substantia nigra pars compacta.

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

197 s in STN, globus pallidus externa (GPe), and substantia nigra pars reticular (SNr), and disrupted bet

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

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

200 of studies have shown that inhibition of the substantia nigra pars reticulata (SNpr) attenuates seizu

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

202 ay, resulting in unbalanced responses in the substantia nigra pars reticulata (SNr) and suggesting a

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

204 l activation of CDt-derived terminals in the substantia nigra pars reticulata (SNr) inhibits SNr neur

205 odent basal ganglia (BG) output nucleus, the substantia nigra pars reticulata (SNr) is well positione

206 n of parvalbumin-positive (PV(+)) neurons in substantia nigra pars reticulata (SNR), accompanied with

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

208 anglia GABAergic output in the midbrain, the substantia nigra pars reticulata (SNr), shows movement-r

209 Excitation of GABAergic cells in the substantia nigra pars reticulata (SNr), the main output

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

211 The substantia nigra pars reticulata (SNr), where the basal

212 unction by acting on 5-HT2C receptors in the substantia nigra pars reticulata (SNr), which in turn in

213 BA neurons, with ~50% of GABA neurons in the substantia nigra pars reticulata (SNr), ~30% in the VTA,

214 ors are coregulated by shared neurons in the substantia nigra pars reticulata (SNr).

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

216 nd that excitation of GABAergic cells in the substantia nigra pars reticulata blocks signaled active

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

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

219 proper GABAergic neuronal migration into the substantia nigra pars reticulata.

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

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

222 For each voxel in the substantia nigra, probability map of controls, correlati

223 specifically in dopaminergic neurons of the substantia nigra, produced cataleptic behaviours associa

224 he finding of increased NM-MRI signal in the substantia nigra provides additional insight into the pa

225 Substantia nigra, putamen, and cortical p11 protein leve

226 The identified modules were derived from the substantia nigra, putamen, frontal cortex, and white mat

227 Conclusion In patients with stroke, greater substantia nigra R2*, likely reflective of greater iron

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

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

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

231 sh the physiological trajectory by which the substantia nigra reticulata (SNr) transitions from the h

232 led us to assess voxel-wise modifications of substantia nigra's morphology in vivo in humans, includi

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

234 Based on the aligned substantia nigra segmentations using a study-specific br

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

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

237 volved in T cell trafficking, in vivo in the substantia nigra (SN) and the serum of 1-methyl-4-phenyl

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

239 of N-glycans isolated from the striatum and substantia nigra (SN) can give an insight into the estab

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

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

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

243 ression levels and cell type patterns in the substantia nigra (SN) from 53 donors with and without PD

244 onsistent with the expression profile of the substantia nigra (SN) from PD patients, analyzed post mo

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

246 Background The substantia nigra (SN) is suspected to be affected after

247 llular distribution of neutral lipids in the substantia nigra (SN) of Parkinson's disease (PD) patien

248 Dopamine neurons in the substantia nigra (SN) pars compacta are selectively lost

249 also differentiated DA neurons in the medial substantia nigra (SN) projecting either to dorsal or ven

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

251 The substantia nigra (SN) provides the largest dopaminergic

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

253 man mutant alpha-synuclein (A53T) in the rat substantia nigra (SN) to produce degeneration of SN dopa

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

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

256 n single-nuclei transcriptomic atlas for the substantia nigra (SN), generated by sequencing approxima

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

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

259 he switching neurons make projections to the substantia nigra (SN), ventral tegmental area (VTA) and

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

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

262 umulates with age in dopamine neurons of the substantia nigra (SN).

263 ild-type alpha-syn unilaterally into the rat substantia nigra (SN).

264 eduction in GLAST/GLT-1 expression in murine substantia nigra (SN).

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

266 rons in the ventral tegmental area (VTA) and substantia nigra (SNc) encode reward prediction errors (

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

268 y loss of dopaminergic neurons (DaNs) in the substantia nigra (SNc), whereas DaNs in the neighboring

269 In particular, the dopaminergic substantia nigra (SNc)-related nigrostriatal pathway is

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

271 robust inhibitory projections to the lateral substantia nigra (SNL) that contribute to appetitive and

272 s, secreted by microglia, in the ipsilateral substantia nigra, the main region in the brain affected

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

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

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

276 sed by a loss of dopaminergic input from the substantia nigra to the caudate nucleus and the putamen.

277 depression, anxiety, or hyperechogenicity on substantia nigra ultrasound.

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

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

280 with slower baseline gait speed (346 of 1807 substantia nigra-ventral tegmental area (SN-VTA) voxels,

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

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

283 ocalization in brain areas projecting to the substantia nigra/ventral tegmental area.

284 cumulates in dopamine neurons of the VTA and substantia nigra via nifedipine-sensitive Ca(2+) channel

285 pose To evaluate quantitative measurement of substantia nigra volume by using MRI to support clinical

286 s before disease diagnosis, and 23.1% of the substantia nigra volume was lost at the time of diagnosi

287 internal reference was used for hyperintense substantia nigra volumetry normalized to intracranial vo

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

289 with CUD, greater D3R-related binding in the substantia nigra was associated with improved performanc

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

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

292 The bilateral substantia nigra was evaluated by two neuroradiologists

293 potential for caudate nucleus, putamen, and substantia nigra was evaluated using the simplified refe

294 healthy control subjects, the volume of the substantia nigra was progressively reduced for increasin

295 the probability of a voxel belonging to the substantia nigra were calculated for patients with vario

296 ensive streaking and low signal intensity in substantia nigra were seen in two individuals.

297 tein colocalizes with DA neurons in the male substantia nigra, where it regulates DA biosynthesis and

298 dicates that dopaminergic neurons in lateral substantia nigra, which innervate the sensorimotor stria

299 in the death of dopaminergic neurons in the substantia nigra, which is the root cause of dopamine de

300 esulted in Lewy pathology in the ipsilateral substantia nigra with significant reduction (-29.30%) of