ライフサイエンスコーパス: substantia

1 brain regions-the frontal gyrus, the lateral substantia, and the medial substantia in PD patients.

2 yrus, the lateral substantia, and the medial substantia in PD patients.

3 ut to the magnocellular preoptic nucleus and substantia innominata (MCPO/SI) in mice and determined t

4 f glutamatergic and GABAergic neurons of the substantia innominata (SI) and magnocellular preoptic ar

5 BF, including the caudal globus pallidus and substantia innominata and moderate input from the horizo

6 monstrate that electrical stimulation of the substantia innominata of the basal forebrain phase shift

7 gonal band, magnocellular preoptic area, and substantia innominata).

8 septum, bed nucleus of the stria terminalis, substantia innominata, various thalamic and hypothalamic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

30 The substantia nigra (SN) provides the largest dopaminergic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 Substantia nigra dopamine neurons are involved in behavi

73 Substantia nigra dopamine neurons fire tonically resulti

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

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

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

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

78 20N VPS35 induces the marked degeneration of substantia nigra dopaminergic neurons and axonal patholo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 Substantia nigra pars compacta (SNc) dopamine neurons an

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

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

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

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

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

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

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

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

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

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

140 The substantia nigra pars compacta (SNc) projects specifical

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 Studying mouse substantia nigra pars compacta dopaminergic neurons both

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

236 The bilateral substantia nigra was evaluated by two neuroradiologists

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 Substantia nigra, putamen, and cortical p11 protein leve

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

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

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

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

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

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

262 pigmented dopaminergic neuronal count in the substantia nigra.

263 ed connectivity between ventral striatum and substantia nigra.

264 imarily in the dopaminergic neurons of human substantia nigra.

265 after lesioning dopaminergic neurons of the substantia nigra.

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

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

268 elective loss of dopaminergic neurons in the substantia nigra.

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

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

271 xonal transport of neurturin from putamen to substantia nigra.

272 ffects on residual dopaminergic cells in the substantia nigra.

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

274 was measured in dopaminergic cells from the substantia nigra.

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

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

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

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

279 ependent currents in dopamine neurons in the substantia nigra.

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

281 gressive loss of dopaminergic neurons in the substantia nigra.

282 induced loss of dopaminergic neurons in the substantia nigra.

283 yrosine hydroxylase-immunostained neurons in substantia nigra.

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

285 essive loss of dopaminergic neurons from the substantia nigra.

286 bellar systems and dopaminergic cells of the substantia nigra.

287 degeneration of dopaminergic neurons in the substantia nigra.

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

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

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

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

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

293 lidus but decrease in entopeduncular nucleus/substantia nigra.

294 elective loss of dopaminergic neurons of the substantia nigra.

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

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

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

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

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

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