ライフサイエンスコーパス: nigra

1 s accumbens, globus pallidus, and substantia nigra).

2 d loss of dopamine neurons in the substantia nigra.

3 assing ventral tegmental area and substantia nigra.

4 opamine-containing neurons of the substantia nigra.

5 ing dopaminergic neurons from the substantia nigra.

6 from the most likely seed region, substantia nigra.

7 , frontal cortex, cerebellum, and substantia nigra.

8 the caudate-putamen, striatum and substantia nigra.

9 e from both ventral tegmentum and substantia nigra.

10 lective D-serine reduction in the substantia nigra.

11 amygdala, striatum, pulvinar, and substantia nigra.

12 of dopaminergic neurons from the substantia nigra.

13 ss of dopaminergic neurons in the substantia nigra.

14 ed in dopaminergic cells from the substantia nigra.

15 SNs) or indirectly (iMSNs) to the substantia nigra.

16 on of dopaminergic neurons in the substantia nigra.

17 e SVPE signal was detected in the substantia nigra.

18 roxylase (TH)-positive neurons of substantia nigra.

19 gions of the ventral pallidum and substantia nigra.

20 ss of dopaminergic neurons in the substantia nigra.

21 dopaminergic (DA) neurons in the substantia nigra.

22 ecrease in entopeduncular nucleus/substantia nigra.

23 ss of dopaminergic neurons of the substantia nigra.

24 healthy controls, but not in the substantia nigra.

25 g a voxelwise analysis within the substantia nigra.

26 l Iba1-positive population in the substantia nigra.

27 alized in distinct regions of the substantia nigra.

28 rols neuronal migrations into the substantia nigra.

29 n aggregates into the striatum or substantia nigra.

30 where CERE120 was directly delivered to the nigra.

31 lamus (0.26% increase, P < .001), substantia nigra (0.25% increase, P = .01), red nucleus (0.25% incr

32 y loss of dopamine neurons in the substantia nigra(1).

33 y, we confirmed lower SV2A in the substantia nigra (-17%; p < 0.005) and nonsignificant findings in t

34 ials in the caudate, putamen, and substantia nigra (4.9, 4.9, and 1, respectively) were similar to th

35 group exhibited lower SV2A in the substantia nigra (-45%; p < 0.001), red nucleus (-31%; p = 0.03), a

36 ed alpha-synuclein in ipsilateral substantia nigra and adjacent to the injection site.

37 rvival of dopaminergic neurons in substantia nigra and an increased number of microglia expressing ma

38 ented dopaminergic neurons in the substantia nigra and associated striatal deafferentation.

39 on of dopaminergic neurons in the substantia nigra and cholinergic neurons in the dorsal motor nucleu

40 rexpressed in Parkinson's disease substantia nigra and confers drug-inducible neuroprotection from ox

41 gene regulatory structures in the substantia nigra and determine key regulators of the PD transcripto

42 drove continuous T cell infiltration to the nigra and incessant glial inflammation.

43 DNER is highly expressed in substantia nigra and is an activator of the NOTCH1 pathway which ha

44 were between ADGRV1 and GRIK2 in substantia nigra and medullary inferior olivary nucleus, and betwee

45 d normal controls (n = 13) in the substantia nigra and putamen.

46 ost-mortem histology of the human substantia nigra and radiotracer studies of the human striatum.

47 o PDE10A in striatoentopeduncular/substantia nigra and striatopallidal pathways might tightly interac

48 inates at least from two sources, substantia nigra and thalamic reticular nucleus.

49 and in globus pallidus, putamen, substantia nigra and the dentate nucleus compared to PD and control

50 ss of dopaminergic neurons in the substantia nigra and the formation of Lewy body inclusions containi

51 minergic (DAergic) neurons in the substantia nigra and the gradual depletion of dopamine (DA).

52 lanin-sensitive MRI signal in the substantia nigra and their relation to clinical scores of disease s

53 posterolateral motor areas of the substantia nigra and then progressed to more medial areas of this r

54 ections to entopeduncular nucleus/substantia nigra and to external globus pallidus.

55 s effect was not reflected in the substantia nigra and ventral tegmental area (SN/VTA), medial tempor

56 ed ~3-fold in the midbrain area (substantial nigra and ventral tegmental area) in Taar1 KO compared w

57 rich midbrain nuclei, such as the substantia nigra and ventral tegmental area, also exhibited load-de

58 midbrain region, encompassing the substantia nigra and ventral tegmental area, in 18 daily smokers (7

59 droxylase-positive neurons in the substantia nigra, and attenuated the decrease of striatal dopamine

60 gic neurons of the basal ganglia, substantia nigra, and ventral tegmental area (VTA) where they regul

61 ated from postmortem PD patients' substantia nigra; and (b) leucine-rich repeat kinase 2 (LRRK2) gene

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

63 vitro study confirmed that the fruits of S. nigra are capable of protecting colonic cells against th

64 l in ventrolateral regions of the substantia nigra (area under the receiver operating characteristic

65 idate free water in the posterior substantia nigra as a progression marker in Parkinson's disease, an

66 t in globus pallidus internus and substantia nigra at 6 months and remained so at 18 months.

67 al structures including striatum, substantia nigra, basal forebrain (BF), pedunculopontine nucleus (P

68 ery), and to the putamen plus the substantia nigra bilaterally in the second (8 years post-surgery).

69 ethmoid sinus, clivus, meninges, substantia nigra, but not the basal ganglia or choroid plexus.

70 on of dopaminergic neurons in the substantia nigra causes the motor symptoms of Parkinson's disease.

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

72 analyzed expression in the human substantia nigra, comparing cell states in specific donors and rela

73 lls of the ventral tegmental area/substantia nigra complex.

74 he striatum, while only few adult substantia nigra DA neurons have this capacity.

75 ver, direct stimulation of VTA or substantia nigra dopamine cell bodies failed to induce food approac

76 tral tegmental area and decreased substantia nigra dopamine neuron population activity.

77 Substantia nigra dopamine neurons have been implicated in the initi

78 as shown by increased survival of substantia nigra dopamine neurons, integrity of striatal dopaminerg

79 sfunction have been implicated in substantia nigra dopaminergic neurodegeneration in Parkinson's dise

80 inhibition.SIGNIFICANCE STATEMENT Substantia nigra dopaminergic neurons can be divided into two popul

81 nduces the robust degeneration of substantia nigra dopaminergic neurons, a pathological hallmark of P

82 nts glutamate accumulation in the substantia nigra during hyperlocomotive states.

83 key brain regions, including the substantia nigra, entopeduncular nucleus, and nucleus accumbens she

84 c liposomes containing black mulberry (Morus nigra) extract (BME) were prepared by high pressure homo

85 nscriptomic data from putamen and substantia nigra from 117 human brains, interrogating regulation at

86 etric measurement of hyperintense substantia nigra from magnetization transfer-prepared T1-weighted M

87 Microwave assisted extraction (MAE) of Morus nigra fruits was optimized in order to elicit process pa

88 nced technique to obtain extracts from Morus nigra fruits with higher bioactive content and activity.

89 r the ictal increase in firing of substantia nigra GABAergic neurons.

90 e loss of dopamine neurons in the substantia nigra has been known for the last 50.

91 T1-weighted MRI volumetry of the substantia nigra helped differentiate the stages of Parkinson disea

92 Substantia nigra hyperechogenicity, olfactory loss, depression, ort

93 ar in free water in the posterior substantia nigra in a large cohort of de novo patients with Parkins

94 the targeted globus pallidus and substantia nigra in a time-dependent manner.

95 in other brain regions beyond the substantia nigra in Parkinson's disease, multiple system atrophy, a

96 e ratio between the volume of the substantia nigra in patients with Parkinson's disease relative to t

97 and the ventral tegmental area and subtantia nigra in the ventral mesencephalon.

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

99 free water level in the posterior substantia nigra increased over 1 year in de novo Parkinson's disea

100 66017 when microinjected into the substantia nigra, infralimbic cortex, BLA, and CeA.

101 lectively, our results suggest that amygdala-nigra interactions represent a previously unappreciated

102 cal and functional subdivision of substantia nigra into dorsal and ventral tiers and striatal nuclei

103 ses and two anthocyanidin reductases from P. nigra involved in catalyzing the last steps of flavan-3-

104 t a hyperintense subregion of the substantia nigra involved in the degeneration process of Parkinson

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

106 Sambucus nigra is one of the richest sources of anthocyanins and

107 . cathayensis, J. hindsii, J. microcarpa, J. nigra, J. sigillata and Pterocarya stenoptera) produced

108 Morus nigra L. is a beneficial food due to rich phenolic compo

109 Elderberry (EDB) Sambucus nigra L. is one of the oldest medicinal plants which is

110 ed into the commercial hybrid poplar Populus nigra L. x P. maximowiczii A.

111 nifera L. var. Albarino) and mulberry (Morus nigra L.) seeds pomace were characterized in terms of to

112 prenoids profile from elderflowers (Sambucus nigra L.) was established for two cultivars by multidime

113 is highly expressed in the adult substantia nigra, leading us to investigate a role of the netrin-1/

114 n of Fc receptors, was evaluated by Sambucus nigra lectin blotting.

115 Erythrina cristagalli lectin (ECL), Sambucus nigra lectin, and Phaseolus vulgaris Erythroagglutinin (

116 od and treadmill tests, caused by substantia nigra lesioning in mice.

117 of Parkinson's disease within the substantia nigra module.

118 brown (Brassica juncea), and black (Brassica nigra) mustard seeds are still scarce in the literature.

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

120 ers to 'Spatiotemporal changes in substantia nigra neuromelanin content in Parkinson's disease', by B

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

122 In the substantia nigra, neurturin expression was detected in 9.8-18.95% a

123 the burden of alpha-syn in DA neurons in the nigra of A53T transgenic (A53T-Tg) mouse.

124 n of human alpha-synuclein in the substantia nigra of aged (18 to 21-month-old) L444P Gba1 mice.

125 of macaque monkeys, close to the substantia nigra of both sides.

126 t silencing netrin-1 in the adult substantia nigra of mice induces DCC cleavage and a significant los

127 ed in dopaminergic neurons of the substantia nigra of Parkinson's disease (PD) patients and decreased

128 to be increased in the posterior substantia nigra of Parkinson's disease compared with controls at a

129 significantly upregulated in the substantia nigra of patients with Parkinson's disease.

130 regated synuclein deposits in the substantia nigra of patients with Parkinson's disease.

131 ctivity have been observed in the substantia nigra of PD patients, and loss of Parkin results in the

132 ontaining dopaminergic neurons in substantia nigra of PD patients.

133 er a (RGMa) is upregulated in the substantia nigra of PD patients.

134 ynuclein toxicity in vivo, in the substantia nigra of rats.

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

136 very of human alpha-SYN into their sustantia nigra or by treatment with l-DOPA, suggesting that alpha

137 ressed in striatoentopeducuncular/substantia nigra or striatopallidal pathways, respectively.

138 rtical glutamate neurons into the substantia nigra or striatum of a mouse PD model and found extensiv

139 he activation of microglia in the substantia nigra par compacta of MPTP-treated mice.

140 d dopaminergic neurons in the rat substantia nigra pars compact, increases the recruitment of endogen

141 ate to form the laterally-located substantia nigra pars compacta (SN) and medially-located ventral te

142 ars reticulata (SNr), which in turn inhibits nigra pars compacta (SNc) DAergic neurons.

143 ergic neurons (DAs) of the rodent substantia nigra pars compacta (SNc) display varied electrophysiolo

144 nerative disease characterized by substantia nigra pars compacta (SNc) dopamine (DA) neuron loss and

145 Substantia nigra pars compacta (SNc) dopamine neurons and their tar

146 ior studies have established that substantia nigra pars compacta (SNc) dopamine neurons are a key nod

147 jor factor underlying the loss of substantia nigra pars compacta (SNc) dopaminergic neurons in Parkin

148 Burst spiking in substantia nigra pars compacta (SNc) dopaminergic neurons is a key

149 vior that depend on the firing of substantia nigra pars compacta (SNc) dopaminergic neurons, we ident

150 egion homologous to the mammalian substantia nigra pars compacta (SNc) evokes increasing activation o

151 dopaminergic (DA) neurons of the substantia nigra pars compacta (SNc) govern movements requires a de

152 unctional heterogeneity among the substantia nigra pars compacta (SNc) neurons.

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

154 ventral tegmental area (VTA) and substantia nigra pars compacta (SNc), no clear evidence for separat

155 opaminergic neurons (DaNs) of the substantia nigra pars compacta (SNc), resulting in the characterist

156 sease (PD)-related changes in the substantia nigra pars compacta (SNc), the key pathological loci.

157 t has been suggested that, in the substantia nigra pars compacta (SNc), the pacemaking relies more on

158 t loss of dopamine neurons in the substantia nigra pars compacta (SNc).

159 ventral tegmental area (VTA) and substantia nigra pars compacta (SNc).

160 es of dopamine neurons within the substantia nigra pars compacta (SNc).

161 s of dopamine (DA) neurons in the substantia nigra pars compacta (SNc).

162 tects dopaminergic neurons of the substantia nigra pars compacta (SNpc) against 6-OHDA and MPTP.

163 dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) and of noradrenergic neurons

164 ons onto these neurons in the rat substantia nigra pars compacta (SNpc) and ventral tegmental area (V

165 y loss of dopamine neurons in the substantia nigra pars compacta (SNpc) and widespread aggregates of

166 higher centers, compromising the substantia nigra pars compacta (SNpc) and, later, the cerebral cort

167 Neuronal loss in the substantia nigra pars compacta (SNpc) in Parkinson disease (PD) is

168 ow that optogenetic activation of substantia nigra pars compacta (SNpc) neurons alleviates parkinsoni

169 ergic (DA) neurons at the ventral substantia nigra pars compacta (SNpc) preferentially degenerate in

170 dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) remains to be answered.

171 , reduced dopaminergic neurons in substantia nigra pars compacta (SNpc), and SNCA mice were more vuln

172 t loss of dopaminergic neurons in substantia nigra pars compacta (SNpc), and there was no loss of dop

173 opaminergic neurons (DANs) in the substantia nigra pars compacta (SNpc), decrease of dopamine (DA) tr

174 signal intensity loss within the substantia nigra pars compacta (SNpc), locus coeruleus, and ventral

175 nin-containing cell levels in the substantia nigra pars compacta and nigrostriatal terminal density i

176 c dopamine neurons located in the substantia nigra pars compacta and the ventral tegmental area, whic

177 peduncular nucleus, raphe nuclei, substantia nigra pars compacta and ventral tegmental area homologs,

178 Dopamine neurons in the substantia nigra pars compacta and ventral tegmental area regulate

179 g both ventral tegmental area and substantia nigra pars compacta DA neurons in the post-reward period

180 or distance from the soma in rat substantia nigra pars compacta dopaminergic neurons.

181 ression of alpha-synuclein in the substantia nigra pars compacta impacts visual processing in a well-

182 ation of nigrostriatal neurons of substantia nigra pars compacta in Parkinson's disease represents th

183 om the ventral tegmental area and substantia nigra pars compacta innervate the majority of the cortex

184 on of dopaminergic neurons in the substantia nigra pars compacta is the primary cause for motor sympt

185 o how neuron subtypes outside the substantia nigra pars compacta may be compensating at a molecular l

186 type B (trkB) receptor occurs in substantia nigra pars compacta neurons and is required for neuropro

187 vulnerable dopaminergic (DAergic) substantia nigra pars compacta neurons, only select downregulation

188 In vivo data from the cortex and substantia nigra pars compacta of aged LRRK2 transgenic animals rev

189 on of dopaminergic neurons in the substantia nigra pars compacta portion of the brain.

190 fraction from frontal cortex and substantia nigra pars compacta tissue, isolated by several filtrati

191 ration of dopamine neurons of the substantia nigra pars compacta, a deficit in dopamine neurotransmis

192 nd in dopaminergic neurons of the substantia nigra pars compacta, a susceptible brain region in PD.

193 neuronal loss and gliosis in the substantia nigra pars compacta, without Lewy bodies.

194 la, dorsal raphe nucleus, and the substantia nigra pars compacta.

195 l loss of dopamine neurons in the substantia nigra pars compacta.

196 nine was infused locally into the substantia nigra pars compacta.

197 not in ventral tegmental area or substantia nigra pars lateralis, consistently represented the onset

198 lobus pallidus externa (GPe), and substantia nigra pars reticular (SNr), and disrupted beta band osci

199 caudal-dorsal-lateral part of the substantia nigra pars reticulata (cdlSNr), directly or indirectly t

200 Hz range in LFPs recorded in the substantia nigra pars reticulata (SNpr) and motor cortex (MCx) in t

201 have shown that inhibition of the substantia nigra pars reticulata (SNpr) attenuates seizures, yet th

202 e pedunculopontine nucleus to the substantia nigra pars reticulata (SNr) act on muscarinic acetylchol

203 ng in unbalanced responses in the substantia nigra pars reticulata (SNr) and suggesting a mechanism f

204 of the basal ganglia through the substantia nigra pars reticulata (SNr) controls active avoidance.

205 n of CDt-derived terminals in the substantia nigra pars reticulata (SNr) inhibits SNr neurons.

206 ganglia (BG) output nucleus, the substantia nigra pars reticulata (SNr) is well positioned to impact

207 bumin-positive (PV(+)) neurons in substantia nigra pars reticulata (SNR), accompanied with anxiety-li

208 reach their midbrain target, the substantia nigra pars reticulata (SNr), at E14 in the mouse with a

209 ergic output in the midbrain, the substantia nigra pars reticulata (SNr), shows movement-related neur

210 itation of GABAergic cells in the substantia nigra pars reticulata (SNr), the main output of the basa

211 We recorded from the substantia nigra pars reticulata (SNR), the major basal ganglia out

212 The substantia nigra pars reticulata (SNr), where the basal ganglia (BG

213 acting on 5-HT2C receptors in the substantia nigra pars reticulata (SNr), which in turn inhibits nigr

214 with ~50% of GABA neurons in the substantia nigra pars reticulata (SNr), ~30% in the VTA, and ~70% i

215 egulated by shared neurons in the substantia nigra pars reticulata (SNr).

216 ipsilateral and the contralateral substantia nigra pars reticulata (SNr).

217 itation of GABAergic cells in the substantia nigra pars reticulata blocks signaled active avoidance b

218 ergic output projections from the substantia nigra pars reticulata to the deep layers of the superior

219 ergic neuronal migration into the substantia nigra pars reticulata.

220 se in free water in the posterior substantia nigra predicts subsequent long-term progression on the H

221 ections to entopeduncular nucleus/substantia nigra, preferentially expressing D1 receptors that stimu

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

223 ly in dopaminergic neurons of the substantia nigra, produced cataleptic behaviours associated with im

224 of increased NM-MRI signal in the substantia nigra provides additional insight into the pathophysiolo

225 Substantia nigra, putamen, and cortical p11 protein levels were ass

226 ied modules were derived from the substantia nigra, putamen, frontal cortex, and white matter, and we

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

228 s seen in the posterior thalamus, substantia nigra, red nucleus, cerebellar peduncle, colliculi, dent

229 nalyzed MTA1 and TH levels in the substantia nigra region of a large cohort of human brain tissue sam

230 tivity of adult DA neurons in the substantia nigra region.

231 iological trajectory by which the substantia nigra reticulata (SNr) transitions from the healthy to t

232 ssess voxel-wise modifications of substantia nigra's morphology in vivo in humans, including healthy

233 stochemistry analysis for MTA1 in substantia nigra sections revealed that 74.1% of the samples had a

234 ven were found in B. alba, B. juncea, and B. nigra seeds, respectively.

235 Based on the aligned substantia nigra segmentations using a study-specific brain anatomi

236 on of dopaminergic neurons in the substantia nigra (SN) and affected the integrity of the nigrostriat

237 uding dopaminergic neurons of the substantia nigra (SN) and cholinergic neurons of the dorsal motor n

238 cell trafficking, in vivo in the substantia nigra (SN) and the serum of 1-methyl-4-phenyl-1,2,3,6-te

239 inergic (DA) neuronal loss in the substantia nigra (SN) and ventral tegmental area (VTA), supporting

240 ns isolated from the striatum and substantia nigra (SN) can give an insight into the establishment an

241 DBS provides neuroprotection for substantia nigra (SN) dopamine neurons and increases BDNF in the ni

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

243 els and cell type patterns in the substantia nigra (SN) from 53 donors with and without PD, as well a

244 ith the expression profile of the substantia nigra (SN) from PD patients, analyzed post mortem.

245 ventral tegmental area (VTA) and substantia nigra (SN) has been examined at multiple levels.

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

247 ribution of neutral lipids in the substantia nigra (SN) of Parkinson's disease (PD) patients and its

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

249 entiated DA neurons in the medial substantia nigra (SN) projecting either to dorsal or ventral striat

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

251 The substantia nigra (SN) provides the largest dopaminergic input to th

252 y of dopamine (DA) neurons in the substantia nigra (SN) to neurodegenerative stressors causes Parkins

253 alpha-synuclein (A53T) in the rat substantia nigra (SN) to produce degeneration of SN dopamine neuron

254 ctional organization of the human substantia nigra (SN) using diffusion and functional MRI data from

255 udate, putamen, ventral striatum, substantia nigra (SN), and cerebellum were manually drawn on coregi

256 clei transcriptomic atlas for the substantia nigra (SN), generated by sequencing approximately 17,000

257 pha-syn fibril seeds into the rat substantia nigra (SN), in combination with adenoassociated virus (A

258 : the dentate nucleus (DN), pons, substantia nigra (SN), pulvinar thalami, and globus pallidus (GP).

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

260 dopaminergic (DA) neurons in the substantia nigra (SN), which may contribute to their selective dege

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

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

263 lpha-synuclein (alpha-syn) in the substantia-nigra (SN).

264 pha-syn unilaterally into the rat substantia nigra (SN).

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

266 ventral tegmental area (VTA) and substantia nigra (SNc) encode reward prediction errors (RPEs) and a

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

268 opaminergic neurons (DaNs) in the substantia nigra (SNc), whereas DaNs in the neighboring ventral teg

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

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

271 bitory projections to the lateral substantia nigra (SNL) that contribute to appetitive and aversive l

272 We show in Arabidopsis thaliana and Brassica nigra that localized FR enrichment at the lamina tip ind

273 by microglia, in the ipsilateral substantia nigra, the main region in the brain affected in Parkinso

274 to the ventral tegmental area and substantia nigra; the dopamine systems themselves; glutamatergic af

275 reasing TGF-beta signaling in the substantia nigra through adeno-associated virus expressing a consti

276 ilar to those isolated from human substantia nigra tissues.

277 ss of dopaminergic input from the substantia nigra to the caudate nucleus and the putamen.

278 anxiety, or hyperechogenicity on substantia nigra ultrasound.

279 ntrast to dopamine neurons in the substantia nigra, vagal motoneurons do not enhance their excitabili

280 mber of CARTp-ir terminals in the substantia nigra, ventral tegmental area, periaqueductal gray, para

281 baseline gait speed (346 of 1807 substantia nigra-ventral tegmental area (SN-VTA) voxels, P(correcte

282 r binding in D3-rich regions: the substantia nigra/ventral tegmental area (SN/VTA) (+20%; p=0.02), ve

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

284 n dopamine neurons of the VTA and substantia nigra via nifedipine-sensitive Ca(2+) channels.

285 luate quantitative measurement of substantia nigra volume by using MRI to support clinical diagnosis

286 sease diagnosis, and 23.1% of the substantia nigra volume was lost at the time of diagnosis, which wa

287 ference was used for hyperintense substantia nigra volumetry normalized to intracranial volume.

288 reater D3R-related binding in the substantia nigra was associated with improved performance and great

289 that free water in the posterior substantia nigra was elevated in Parkinson's disease compared to co

290 for caudate nucleus, putamen, and substantia nigra was evaluated using the simplified reference tissu

291 ough marked infiltration of T cells into the nigra was found on 1 d of MPTP insult, T cell infiltrati

292 ntrol subjects, the volume of the substantia nigra was progressively reduced for increasing disease s

293 ctional SOT1 allele in black poplar (Populus nigra) was shown to correlate with the absence of salici

294 ility of a voxel belonging to the substantia nigra were calculated for patients with various degrees

295 aking and low signal intensity in substantia nigra were seen in two individuals.

296 lizes with DA neurons in the male substantia nigra, where it regulates DA biosynthesis and voluntary

297 ity of flavan-3-ols in black poplar (Populus nigra), which include both monomers, such as catechin, a

298 t dopaminergic neurons in lateral substantia nigra, which innervate the sensorimotor striatum, are en

299 th of dopaminergic neurons in the substantia nigra, which is the root cause of dopamine deficit in th

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