ライフサイエンスコーパス: nigral

1 There was no correlation between nigral (18)F-AV-1451 volume of distribution and age or t

2 patients showed a 30% mean decrease in total nigral (18)F-AV-1451 volume of distribution compared wit

3 Furthermore, nigral (18)F-dihydroxyphenyl-L-alanine uptake was positi

4 These results suggest that nigral 5-HT, via presynaptic 5-HT1B receptor activation,

5 Nigral 6-hydroxydopamine (6-OHDA) lesions or repeated D2

6 Five or 21 d after nigral 6-OHDA injections or after 3, 7, or 21 d of D2 an

7 of proinflammatory molecules, and suppressed nigral activation of glial cells.

8 of proinflammatory molecules, and suppressed nigral activation of glial cells.

9 of proinflammatory molecules, and suppressed nigral activation of glial cells.

10 ected nigral reduced glutathione, attenuated nigral activation of NF-kappaB, inhibited nigral express

11 ed nigral activation of p21(ras), attenuated nigral activation of NF-kappaB, inhibited nigral express

12 . injection of wild-type NBD peptide reduced nigral activation of NF-kappaB, suppressed nigral microg

13 Oral administration of NaPB reduced nigral activation of p21(ras) and p21(rac), protected ni

14 simvastatin entered into the nigra, reduced nigral activation of p21(ras), attenuated nigral activat

15 In short, these results suggest that (1) nigral activity is highly plastic and modified by the le

16 In the present study, we show that direct nigral administration of a NO donor, SNOG, in the rat pr

17 tein alpha-synuclein present in dopaminergic nigral afferents in the regulation of adult neural stem

18 eport that alpha-SYN present in dopaminergic nigral afferents is essential for the normal cycling and

19 restoration of the DA modulation of striatal-nigral afferents that is lost after degeneration of SN n

20 induced by early selective overexpression of nigral alpha-syn are still a matter of debate.

21 in was also associated with the induction of nigral alpha-synuclein pathology, persistent loss of dop

22 influence of nigral neuronal loss as well as nigral (alpha-synuclein, tau) and striatal (alpha-synucl

23 atment lowers brain tau levels and increases nigral and cortical iron elevation that is closely assoc

24 tg) mouse model, which resembles the striato-nigral and motor deficits of PD.

25 However, whereas nigral and striatal (18)F-dihydroxyphenyl-L-alanine upta

26 In an in vivo imaging study, nigral and striatal dopaminergic function was measured i

27 of functional coupling between the putative nigral and striatal homologues is lacking.

28 reductions in ferroportin and elevations in nigral and striatal iron levels were reverted to levels

29 mpts to stimulate the neurogenic process for nigral and/or striatal dopaminergic restoration by trans

30 ath or dysfunctional neurons due to possible nigral and/or striatal neurodegenerative pathology.

31 9, and caspase 3 pathways is operative in PD nigral apoptosis.

32 In contrast, nigral application of either glutamate receptor antagoni

33 Nigral application of the GABA(A) receptor antagonist bi

34 hronic AMI treatment mediates an increase in nigral BDNF both before and during ongoing degeneration,

35 with the early pathologic involvement of non-nigral brainstem regions in PD, as described by Braak.

36 ensity of striatal TH and highest density of nigral CD45 and phospho-p38 MAPK immunoreactivity observ

37 isease onset most likely exceeds that of the nigral cell bodies and has been estimated to be of the o

38 njury to the nigrostriatal pathway including nigral cell bodies, axons and striatal terminal fields.

39 ining dendrites and clusters of their parent nigral cell bodies.

40 Because these measures correlate with both nigral cell counts and parkinsonian ratings, we suggest

41 aphy (PET) tracers with in vitro measures of nigral cell counts and striatal dopamine in 1-methyl-4-p

42 along with previous work demonstrating that nigral cell counts correlate strongly with parkinsonism

43 (FD, DTBZ, CFT) correlated with stereologic nigral cell counts only for nigral loss<50% (r2=0.84, r2

44 ansporter type 2 (VMAT2), striatal dopamine, nigral cell counts, and parkinsonian motor ratings in th

45 uld provide novel insight into the causes of nigral cell death and meaningful strategies for future t

46 Histology confirmed the absence of nigral cell death with concomitant significant loss of s

47 microglial activation may be involved in the nigral cell degeneration in 6-OHDA induced parkinsonian

48 chondrial dysfunction in the pathogenesis of nigral cell degeneration in Parkinson's disease.

49 oupled to its decreased expression following nigral cell degeneration suggests that it may play an im

50 ian and avian brain focusing on pallidal and nigral cell groups.

51 n be differentiated in vitro: CSM14.1, a rat nigral cell line, and NSC34, a mouse motor neuron cell l

52 asures of nigrostriatal terminal fields when nigral cell loss does not exceed 50%.

53 Striatal dopamine deficiency without nigral cell loss is the most likely explanation for the

54 proved motor and cognition function, rescued nigral cell loss, and improved dopamine metabolism.

55 Following MPTP induced nigral cell loss, Cu,Zn-SOD m-RNA levels were decreased

56 ild reduction in striatal TH staining but no nigral cell loss.

57 nd that APP(-/-) mice develop iron-dependent nigral cell loss.

58 son's disease that preceded other well-known nigral cell-related pathology such as phenotypic downreg

59 ised by the presence of severe pars-compacta nigral-cell loss, and accumulation of aggregated alpha-s

60 ii) >20% bilateral increase in the number of nigral cells expressing the dopamine marker tyrosine hyd

61 t increase of TH protein levels are shown in nigral cells in these mutant mice.

62 The remaining lesioned nigral cells of both minocycline-treated groups were lar

63 The loss of nigral cells was prevented by AG pre-treatment.

64 iased counts of tyrosine hydroxylase-stained nigral cells.

65 lial activation and subsequent protection of nigral cells.

66 experiments demonstrate a role for amygdalo-nigral circuitry in learned modulation of attention to s

67 This new model of nigral DA neuron loss may enable identification of early

68 ure to chronic systemic inflammation induced nigral DA neuron loss measured by unbiased stereology.

69 require an inflammatory stimulus to develop nigral DA neuron loss, low-dose lipopolysaccaride (LPS)

70 environmental trigger may be needed to cause nigral DA neuron loss.

71 pesticide, causes selective degeneration of nigral DA neurons and Parkinson disease-like symptoms in

72 provided approximately 85% protection of the nigral DA neurons and their projections to the striatum

73 in parkin knockout mice suggests that human nigral DA neurons have unique vulnerabilities.

74 in MitoPark mouse striatal brain slices, and nigral DA neurons lacked characteristic pacemaker activi

75 eric and polymeric forms of alpha-syn in the nigral DA neurons of A53T-Tg.

76 rkin function increases the vulnerability of nigral DA neurons to inflammation-related degeneration.

77 ession of human wild-type alpha-synuclein in nigral DA neurons, induced by injection of an adeno-asso

78 in, none of them is selectively expressed in nigral DA neurons.

79 ic and neuritic alpha-syn pathologies in the nigral DA neurons.

80 Nigral DA pathology occurred more slowly in the wt-injec

81 Pallido-ponto-nigral degeneration (PPND), caused by an N279K mutation

82 n is found in PD, with predominantly ventral nigral degeneration and absent or rare Lewy bodies.

83 light on the role of dopamine metabolism in nigral degeneration and Parkinson's disease.

84 Parkinson disease (PD) is associated with nigral degeneration and striatal dopamine deficiency.

85 ny years before the development of prominent nigral degeneration and the associated parkinsonian feat

86 pamine neurotransmission, such as exist with nigral degeneration attending Parkinson's disease.

87 ction and oxidative damage in the absence of nigral degeneration in a genetic mouse model of Parkinso

88 nt A145R/I97T) reduced by 50% the retrograde nigral degeneration induced by a striatal injection of t

89 n, therefore, has been hypothesized to cause nigral degeneration via an aberrant accumulation of its

90 Selective nigral degeneration with inclusion formation provoked by

91 le for solTNF-dependent neuroinflammation in nigral degeneration.

92 bit nigrostriatal deficits in the absence of nigral degeneration.

93 abolic markers for remote effects of striato-nigral degeneration.

94 ing is a clinical correlate of pars compacta nigral degeneration.

95 ntaining projection neurons intermingle with nigral dopamine (DA) neuron dendrites.

96 -phenyl-1,2,3,6-tetrahydropyridine (MPTP) to nigral dopamine (DA) neurons.

97 amine neuron cell survival, and striatal and nigral dopamine and DOPAC levels, were evaluated 2 weeks

98 henyl-1,2,3,6-tetrahydropyridine in terms of nigral dopamine cell death.

99 s UCP2 overexpression decreased MPTP-induced nigral dopamine cell loss.

100 se the critical importance of UCP2 in normal nigral dopamine cell metabolism and offer a novel therap

101 xidative stress in PC12-D2R and immortalized nigral dopamine cells.

102 Nigral dopamine neuron cell survival, and striatal and n

103 e reinnervation of dorsal striatum following nigral dopamine neuron loss induced by unilateral intras

104 sociated with (i) >30% bilateral increase in nigral dopamine neurone cell size; (ii) >20% bilateral i

105 pronounced upregulation and regeneration of nigral dopamine neurones and their processes innervating

106 f dopamine neurons, cells in addition to the nigral dopamine neurons appear to be affected by a 6-OHD

107 excess cellular levels of alpha-synuclein in nigral dopamine neurons are closely linked to a progress

108 Nigral dopamine neurons are transiently activated by hig

109 IGNIFICANCE STATEMENT The frequency at which nigral dopamine neurons discharge action potentials sets

110 through CNTF receptor alpha (CNTFRalpha) on nigral dopamine neurons in both the MPP(+)-lesioned or a

111 mans) negatively correlated with survival of nigral dopamine neurons in multiple system atrophy mice

112 predicts that a approximately 30% decline of nigral dopamine neurons is necessary to cause motor symp

113 The spontaneous tonic discharge activity of nigral dopamine neurons plays a fundamental role in dopa

114 ct against 6-hydroxydopamine-induced loss of nigral dopamine neurons when administered 6 h prior to t

115 load in the striatum, as well as survival of nigral dopamine neurons.

116 utamyl)-lysine crosslink are increased in PD nigral dopamine neurons.

117 uclein contribute to the progressive loss of nigral dopamine neurons.

118 amygdala (CeA) and its connections with the nigral dopamine system have been reported to modulate co

119 rate that the tVTA is a major GABA brake for nigral dopamine systems and nigrostriatal functions, and

120 sease (PD) is defined by the degeneration of nigral dopaminergic (DA) neurons and can be caused by mo

121 pesticide, causes selective degeneration of nigral dopaminergic (DA) neurons and Parkinson's disease

122 The loss of nigral dopaminergic (DA) neurons in idiopathic Parkinson

123 arkinsonism correlates well with the loss of nigral dopaminergic cell bodies but only correlates with

124 xhibit attenuated toxic effects of 6-OHDA on nigral dopaminergic cell counts, striatal dopamine conte

125 yl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigral dopaminergic cell loss and up-regulates HIF-1alph

126 o rats causes progressive motor deficits and nigral dopaminergic cell loss in our laboratories, but t

127 deficits, alpha-synuclein accumulation, and nigral dopaminergic cell loss.

128 Differences in nigral dopaminergic cell number between proteasome inhib

129 rosine hydroxylase staining was conducted in nigral dopaminergic cells from post-mortem tissue from p

130 ) and glutathione peroxidase (GPX) following nigral dopaminergic denervation are unclear.

131 a direct activator of the paraquat-mediated nigral dopaminergic neuronal apoptotic machinery and pro

132 al regions, image uptake was associated with nigral dopaminergic neuronal density (P </= 0.04) but no

133 locomotor deficits, dopamine depletion, and nigral dopaminergic neuronal loss.

134 ), mitochondrial dysfunction associates with nigral dopaminergic neuronal loss.

135 d progressive supranuclear palsy (PSP) where nigral dopaminergic neurones also degenerate.

136 bserved that PKCdelta is highly expressed in nigral dopaminergic neurons and colocalizes with TH.

137 Parkinson's disease (PD) the degeneration of nigral dopaminergic neurons and consequently the nigrost

138 xide levels in cerebellar Purkinje cells and nigral dopaminergic neurons but not cortical neurons, th

139 Inhibitory responses of rat nigral dopaminergic neurons by stimulation of afferents

140 ate that PK2 expression is highly induced in nigral dopaminergic neurons during early stages of degen

141 rmore, PK2 expression increased in surviving nigral dopaminergic neurons from PD brains, indicating t

142 e of melatonin was ineffective in protecting nigral dopaminergic neurons from the neurotoxic effects

143 nd p300 expression also were observed within nigral dopaminergic neurons in alphasyn-transgenic mice.

144 electrically evoked GABAergic inhibition in nigral dopaminergic neurons in C57BL/6J mice.

145 fect motor function or cause degeneration of nigral dopaminergic neurons in control rats.

146 The ability to successfully replace lost nigral dopaminergic neurons in Parkinson's disease (PD)

147 ome analyses of laser-capture microdissected nigral dopaminergic neurons in rats and striatal neurons

148 lase staining was significantly increased in nigral dopaminergic neurons in schizophrenia compared wi

149 (1) characterize the age-related changes in nigral dopaminergic neurons in the EAAC1(-/-) mouse, and

150 n mice has no effect on the vulnerability of nigral dopaminergic neurons in vivo in this model system

151 neurotoxicity, where the LPS-induced loss of nigral dopaminergic neurons in vivo was significantly le

152 tive effects on the survival and function of nigral dopaminergic neurons in which the chronic express

153 mutations alone did not alter the number of nigral dopaminergic neurons nor striatal dopamine levels

154 hat co-localized with alpha-synuclein within nigral dopaminergic neurons of paraquat-treated and alph

155 er from studies reporting mtDNA depletion in nigral dopaminergic neurons of PD patients.

156 Stereological counts of nigral dopaminergic neurons revealed a significantly gre

157 mpensatory neuroprotective PK2 signalling in nigral dopaminergic neurons that could have important th

158 However, the MPTP-induced loss of nigral dopaminergic neurons was significantly attenuated

159 of alpha-syn protein, demise and function of nigral dopaminergic neurons, and extent of gliosis in th

160 -induced cytotoxicity in primary cultures of nigral dopaminergic neurons, and recombinant proSAAS blo

161 is characterized by massive degeneration of nigral dopaminergic neurons, dramatic motor and cognitiv

162 , decrease nigral GDNF, augment the death of nigral dopaminergic neurons, induce the loss of striatal

163 ccharide injection when mice had 30% loss of nigral dopaminergic neurons, showed high efficacy in pro

164 onfirmed the expression of Hba-a2 and Hbb in nigral dopaminergic neurons, striatal gamma-aminobutyric

165 spondingly, rotenone-induced degeneration of nigral dopaminergic neurons, their dendrites, and their

166 ntually as neurotoxic as alpha-synuclein for nigral dopaminergic neurons, whereas gamma-synuclein pro

167 Rotenone induced a severe loss of nigral dopaminergic neurons, which was dramatically atte

168 evel in the axonal projections of substantia nigral dopaminergic neurons.

169 cytoglobin mRNA in transcriptome analyses of nigral dopaminergic neurons.

170 s in affected brain regions, most notably in nigral dopaminergic neurons.

171 is essential for the differentiation of the nigral dopaminergic neurons.

172 s, reduced enkephalin expression, diminished nigral dopaminergic projections, and severe deficits in

173 pamine D1 and D2 receptors following loss of nigral dopaminergic projections.

174 nflammatory reaction and degeneration of the nigral-dopaminergic neuronal system exacerbates motor de

175 ed nigral activation of NF-kappaB, inhibited nigral expression of proinflammatory molecules, and supp

176 ed nigral activation of NF-kappaB, inhibited nigral expression of proinflammatory molecules, and supp

177 nd CD8(+) T cells into the nigra, attenuated nigral expression of proinflammatory molecules, and supp

178 The METH-induced increase in nigral extracellular GABA concentrations was D1 receptor

179 Intra-nigral fetal striatal and VM grafts elicited a significa

180 dialysis to determine the potential roles of nigral GABA and glutamate receptors in the regulation of

181 eurochemical correlates such as the surge of nigral GABA and glutamate, and the reduction of thalamic

182 Blockade of nigral GABA(A) receptors by local bicuculline applicatio

183 -113397 and SNC-80 led to the enhancement of nigral GABA, reduction of nigral Glu, and reduction of t

184 Plateau potentials can be elicited in nigral GABAergic neurons by injection of 500 ms depolari

185 The I(CAN)-mediated plateau potential in nigral GABAergic neurons likely affects the way these ne

186 s unable to cause glial activation, decrease nigral GDNF, augment the death of nigral dopaminergic ne

187 substantia nigra neurons but undetectable in nigral glia.

188 the enhancement of nigral GABA, reduction of nigral Glu, and reduction of thalamic GABA levels, consi

189 show that long-term plasticity at subthalamo-nigral glutamatergic synapses (STN-SNr) sculpting the ac

190 in a patient dying 16 years following fetal nigral grafting.

191 rgery as well as animals that received intra-nigral grafts of fetal cerebellar cortex showed no recov

192 sue into the SN to investigate whether intra-nigral grafts would restore motor function in unilateral

193 We assessed loss of dorsolateral nigral hyperintensity (DNH) on high-field susceptibility

194 We have developed an in vitro model of nigral injury, in which lipopolysaccharide-induced micro

195 ruloplasmin attenuated neurodegeneration and nigral iron elevation in the 1-methyl-4-phenyl-1,2,3,6-t

196 Nigral iron elevation is also a feature of Parkinsonian

197 surprisingly no nigral iron staining was observed.

198 Nigral LB-enriched fractions containing pathological alp

199 into the medial forebrain bundle (MFB, full nigral lesion) as an animal model of Parkinson's disease

200 The native protein is a major component of nigral Lewy bodies in Parkinson's disease, and full-leng

201 r and cognitive alterations, and presence of nigral Lewy bodies, whose main constituent is alpha-synu

202 represent subsystems with the nigro-striato-nigral loop that are affected in human disorders includi

203 ake correlated with nigral neurons only when nigral loss was <50%.

204 with stereologic nigral cell counts only for nigral loss<50% (r2=0.84, r2=0.86, r2=0.87, p<0.001 resp

205 To study the mechanisms by which nigral microglia are activated in PD, the potential role

206 d nigral activation of NF-kappaB, suppressed nigral microglial activation, protected both the nigrost

207 oglia, likely either initiates or aggravates nigral neurodegeneration in Parkinson's disease (PD).

208 hereby leading to persistent and progressive nigral neurodegeneration in PD.

209 tomography to visualize the concentration of nigral neuromelanin in Parkinson's disease and correlate

210 n contrast, the number of melanin-containing nigral neuron number was generally stable across age gro

211 ted at the SN provide faithful correlates of nigral neuronal counts across a full range of lesion sev

212 These results suggest that nigral neuronal damage, regardless of etiology, may rele

213 Similarly, nigral neuronal density was assessed quantitatively.

214 ed participants without PD were assessed for nigral neuronal loss and alpha-synuclein immunopositive

215 s that adjusted for age, sex, and education, nigral neuronal loss and Lewy bodies were both related t

216 signs and pathological findings that include nigral neuronal loss and TDP-43 pathology.

217 We aimed to investigate the influence of nigral neuronal loss as well as nigral (alpha-synuclein,

218 About (1/3) of cases had mild or more severe nigral neuronal loss, and about 17% had Lewy bodies.

219 ly NMD3 (rs34016896; P = .03) was related to nigral neuronal loss, and no associations were detected

220 brains, LRRK2 immunoreactivity localized to nigral neuronal processes is dramatically reduced which

221 armoset SN, and OPN protein was localised to nigral neurones although these were not dopaminergic cel

222 y, may be a contributory factor predisposing nigral neurons

223 alpha-synuclein diffusely accumulated within nigral neurons and anatomically interconnected regions,

224 lular inclusions, Lewy bodies, in substantia nigral neurons and, potentially, in the pathology of Par

225 nths, in contrast to the substantial loss of nigral neurons characteristic of Parkinson's disease.

226 This reduction was significantly greater in nigral neurons containing alpha-synuclein inclusions.

227 ofluorescence was significantly decreased in nigral neurons containing alpha-synuclein-immunoreactive

228 d a significant proportion of Lewy bodies in nigral neurons containing SUMO1 and PIAS2.

229 Melanized nigral neurons expressed lower levels of aldolase C mRNA

230 -localization with histones in the nuclei of nigral neurons from mice exposed to a toxic insult (i.e.

231 ncephalic dopaminergic neurons, dopaminergic nigral neurons from MPTP-treated mice, and autopsied Par

232 ATP13A2 levels are decreased in dopaminergic nigral neurons from patients with PD, in which ATP13A2 m

233 s expressed in tyrosine hydroxylase-positive nigral neurons in mice and humans, protects cells from M

234 -essential role of parkin in the survival of nigral neurons in mice.

235 ficant reductions in the number of GTPCHI-ir nigral neurons in middle age (58.4%) and aged (81.5%) ca

236 nificant reduction in the number of Nurr1-ir nigral neurons in middle-aged (23.13%) and aged (46.33%)

237 Furthermore, the firing of nigral neurons in R1441C KI mice show reduced sensitivit

238 Nigral neurons lacking DJ-1 were less sensitive to the i

239 Loss of melanized nigral neurons lags behind the loss of dopamine markers.

240 However, dysfunctional nigral neurons may have an additional effect on striatal

241 evation of RTP801 we detect in PD substantia nigral neurons may mediate their degeneration and death

242 However, surviving nigral neurons occasionally exhibit LRRK2 immunostaining

243 Tracer uptake correlated with nigral neurons only when nigral loss was <50%.

244 The firing rate of most nigral neurons reflected Cartesian coordinates (either x

245 individual with Parkinson's disease, grafted nigral neurons were found to have Lewy body-like inclusi

246 Levels of expression in nigral neurons were higher than in neurons of the red nu

247 ment showed that the numbers of dopaminergic nigral neurons were significantly reduced by 29% and the

248 In many nigral neurons, I(CAN) is masked by tetraethylammonium-s

249 AAV2-NTN significantly preserved nigral neurons, significantly preserved striatal dopamin

250 (STN-SNr) sculpting the activity patterns of nigral neurons, the main output of the network, is also

251 f phosphorylated alpha-syn from the affected nigral neurons.

252 of endogenous NPCs and protection of mature nigral neurons.

253 aggregated SYN as cytoplasmic inclusions in nigral neurons.

254 BAX levels have been found in a subset of PD nigral neurons.

255 egions and iron accumulation in pallidal and nigral neurons.

256 rminal pathology without significant loss of nigral neurons.

257 with and without the Snell genotype, whereas nigral neuropil aggregates were diminished in bigenic HD

258 However, activation of both nigral NK1 and NK3 receptors appears to be required for

259 d dopamine synthesis capacity is seen in the nigral origin of dopamine neurons as well as their stria

260 g and gnawing behaviors, suggesting that the nigral output pathway plays a significant role in the ex

261 asome system and proteolytic stress underlie nigral pathology in both familial and sporadic forms of

262 development of parkinsonian motor signs and nigral pathology in older persons.

263 INTERPRETATION: Nigral pathology is common in persons without PD and may

264 We tested the hypothesis that nigral pathology is related to parkinsonism in older per

265 The nigral pathology triggered by fibrils in combination wit

266 d form of S129 exacerbates alpha-syn-induced nigral pathology, whereas Ser-129 phosphorylation elimin

267 tive feedback through the cortico-subthalamo-nigral pathway and the striatal feedforward inhibition.

268 a pharmacological blockade of the subthalamo-nigral pathway suppresses seizures).

269 ic transmission along the cortico-subthalamo-nigral pathway while keeping constant the average firing

270 ive feedback provided by the cortico-striato-nigral pathway.

271 oluble alpha-synuclein derived from the same nigral PD tissue.

272 triatum exhibited numerous DA neurons in the nigral piece and robust ingrowth into the striatal piece

273 that pathological impairments of subthalamo-nigral plasticity may enhance BG outputs and thereby con

274 These data suggest that nigral plateau potentials are mediated by a calcium-acti

275 Neocortical-type, but not nigral-predominant or limbic-type Lewy body pathology wa

276 ic strategy to determine whether the dlVP or nigral projections from the NAcore are necessary for coc

277 rease of PDE10A in the striatoentopeduncular/nigral projections might lead to increased intensity and

278 superior colliculus (DLSC), a key target of nigral projections, are required for the emergence of CD

279 tivation of p21(ras) and p21(rac), protected nigral reduced glutathione, attenuated nigral activation

280 Ultrastructural analysis of nigral sections from 6 dpl rats using a beta-amyloid dom

281 The magnitude of the nigral signal loss was smaller than the decrease in stri

282 Whole-cell recording of GABA neurons in nigral slices confirmed that NOP receptor blockade enhan

283 m in birds and mammals, but that patterns of nigral staining have diverged in birds and mammals.

284 iptional downregulation of Hba-a2 and Hbb in nigral, striatal, and cortical neurons.

285 for DJ-1 in the survival and/or function of nigral-striatal neurons.

286 ingly, although PK2 expression is low in the nigral system, its receptors are constitutively expresse

287 grative units within the dopamine-containing nigral system.

288 he present studies determined to what extent nigral tachykinin receptor subtypes contribute to striat

289 sed tachykinin peptides and their respective nigral tachykinin receptors are also in position to infl

290 prevent CD by inhibition of the appropriate nigral target region(s).

291 other terminal field measures correlate with nigral TH immunoreactive (TH-ir) cell counts only when n

292 ls, but by 26 wk the wt alpha-syn group lost nigral TH neurons equivalent to the mutated S129A group

293 immunoreactive (TH-ir) cell counts only when nigral TH-ir cell loss does not exceed 50%.

294 did not affect the release of serotonin from nigral tissue, this drug did enhance dopamine release.

295 Fetal nigral transplantation currently cannot be recommended a

296 Two clinical trials of fetal nigral transplantation failed to meet their primary endp

297 ble-blind, placebo-controlled trial of fetal nigral transplantation.

298 utaneously to rats and quantified substantia nigral tyrosine hydroxylase-positive dopaminergic neuron

299 ween symptom dominant side and contralateral nigral volume of distribution.

300 echanism whereby LRRK2 mutants contribute to nigral vulnerability remains unclear.