ライフサイエンスコーパス: SNpc

1 ) neurons in substantia nigra pars compacta (SNpc).

2 urons in the substantia nigra pars compacta (SNPC).

3 ic neurons in the substantia nigra compacta (SNpc).

4 urons of the substantia nigra pars compacta (SNpc).

5 urons in the substantia nigra pars compacta (SNpc).

6 urons in the substantia nigra pars compacta (SNpc).

7 inergic neuron loss in the substantia nigra (SNpc).

8 urons of the substantia nigra pars compacta (SNpc).

9 urons in the substantia nigra pars compacta (SNpc).

10 nd astrocytes expressed iNOS in the lesioned SNpc.

11 adult number of dopaminergic neurons in the SNpc.

12 V neurons receive inputs from neurons of the SNpc.

13 stantial loss of dopaminergic neurons in the SNpc.

14 s in cell lines, as well as in mouse and rat SNpc.

15 duced accumulation of pSyn inclusions in the SNpc.

16 clein transgenic mice was conserved in human SNpc.

17 ad an increase in BrdU-positive cells in the SNpc.

18 euron numbers and BrdU-positive cells in the SNpc.

19 ns of all dopaminergic nuclei, including the SNpc.

20 y cause the selective death of DA neurons in SNpc.

21 TRA-1 targeting causes ectopic expression of snpc-1.3 and male piRNAs during oogenesis.

22 Binding of SNPC-1.3 at male piRNA loci drives spermatogenic piRNA t

23 SNPC-1.3 colocalizes with the core piRNA transcription f

24 Thus, sexually dimorphic regulation of snpc-1.3 expression coordinates male and female piRNA ex

25 Loss of snpc-1.3 leads to depletion of male piRNAs and defects i

26 regulator of sex determination, binds to the snpc-1.3 promoter and represses its expression during oo

27 Here we identify SNPC-1.3, a male germline-enriched variant of a conserve

28 We suggest that SNPC-4 binding establishes a positive expression environ

29 SNPC-4 exhibits an atypical widely distributed binding p

30 SNPC-4 localization is mutually dependent with localizat

31 es with the core piRNA transcription factor, SNPC-4, in nuclear foci of the male germline.

32 We show that C. elegans SNPC-4, the Myb-like DNA-binding subunit of the small nu

33 ntains piRNA silencing-defective 1 (PRDE-1), SNPC-4, twenty-one-U fouled-up 4 (TOFU-4), and TOFU-5.

34 ermatogenic piRNA transcription and requires SNPC-4.

35 n, -83%; P < .001), followed by the anterior SNpc (-49%; P < .001) and the locus coeruleus (-37%; P <

36 how that the substantia nigra pars compacta (SNpc), a brain region where dopamine (DA) cell degenerat

37 ice, there is an up-regulation of Bax in the SNpc after MPTP administration and a decrease in Bcl-2.

38 urons of the substantia nigra pars compacta (SNpc) against 6-OHDA and MPTP.

39 wever, in relationship to its potency in the SNPC, (+)-AJ76 was more potent than haloperidol in the C

40 rons of the substantia nigra, pars compacta (SNpc) akin to what is observed in Parkinson disease (PD)

41 lanin volume loss of the posterior and whole SNpc allowed the best differentiation of patients with P

42 des the mechanistic basis for explaining how SNpc alterations may lead to a high rate of constipation

43 s MPTP-induced dopaminergic neuronal loss in SNpc and nigrostriatal nerve-fiber loss.

44 nsient loss of the dopaminergic phenotype in SNpc and now report that this loss recovers by 90 d afte

45 s (LBs) are abnormal inclusions found in the SNpc and other neurons of these patients.

46 mixed genomes and analyzed number of DNs in SNpc and striatal axonal swellings in 120 F2-En1+/- 17 w

47 ents MPTP-induced activation of microglia in SNpc and striatum and the expression of the cytotoxic me

48 Cop-1 immune cells showed NAA levels, in the SNpc and striatum, nearly equivalent to PBS-treated anim

49 totic protein Bax is highly expressed in the SNpc and that its ablation attenuates SNpc developmental

50 ng rates in dopaminergic neurons in both the SNPC and the CN.

51 of alpha-syn in 2 transplantation sites: the SNpc and the striatum.

52 r N-methyl-d-aspartate microinjection in the SNpc and/or optogenetic stimulation of nigro-vagal termi

53 urons in the substantia nigra pars compacta (SNpc) and by the accumulation of misfolded alpha-synucle

54 sions in the substantia nigra pars compacta (SNpc) and cortical areas, STN DBS did not impact PFF-ind

55 urons in the substantia nigra pars compacta (SNpc) and of noradrenergic neurons in the locus coeruleu

56 urons in rat substantia nigra pars compacta (SNPC) and postsynaptic type II neurons in the anterior c

57 ished in the substantia nigra pars compacta (SNpc) and striatum, regions most affected in human disea

58 opaminergic neurons in the substantia nigra (SNpc) and the subsequent loss of their projecting nerve

59 s in the rat substantia nigra pars compacta (SNpc) and ventral tegmental area (VTA), and compared the

60 urons in the substantia nigra pars compacta (SNpc) and widespread aggregates of the protein alpha-syn

61 romising the substantia nigra pars compacta (SNpc) and, later, the cerebral cortex.

62 c neurons in substantia nigra pars compacta (SNpc), and SNCA mice were more vulnerable.

63 c neurons in substantia nigra pars compacta (SNpc), and there was no loss of dopaminergic neurites in

64 y in the activity of dopaminergic neurons in SNpc, and improvement in the motor function at the behav

65 gest that, just as in other species, the DH, SNpc, and POA might be involved in the expression of soc

66 connects the brainstem vagal nuclei and the SNpc, and to determine whether this pathway is compromis

67 (QA) dramatically enhances the magnitude of SNpc apoptosis and results in a lower number of adult SN

68 Bcl-2 attenuates both natural and QA-induced SNpc apoptosis.

69 Some, but not all of the SNpc apoptotic neurons still express their phenotypic ma

70 urons in the substantia nigra pars compacta (SNpc) are greatly needed to effectively change the debil

71 plasticity leading to neuroprotection in the SNpc as a result of STN-DBS.

72 n apoptosis and elevated microgliosis in the SNpc as well as decreases in DA terminals in the striatu

73 urons in the substantia nigra pars compacta (SNpc) as seen in Parkinson's disease.

74 An unexpected elasticity is observed for the SNPC assemblies with a high modulus that is maintained a

75 urons in the substantia nigra pars compacta (SNpc) at the ages of 20 and 24 months.

76 The binding studies show that DiC(6)SNPC binds cooperatively to two sites on group IA PLA(2)

77 laced tracers in the dorsal vagal complex or SNpc; brainstem and midbrain were examined for tracer di

78 cells in the substantia nigra pars compacta (SNpc), but this difference was significant only among ma

79 ress response in dopaminergic neurons of the SNpc, but not in other brain regions.

80 urons of the substantia nigra pars compacta (SNpc) by regulating the magnitude of the first phase of

81 Ghrelin binds to SNpc cells, electrically activates SNpc DA neurons, incr

82 h more potent than pramipexole in inhibiting SNPC cells, PNU-91356A, a D2-preferring agonist, did not

83 PLA signal was reduced in distal neurites of SNpc compared to VTA neurons.

84 urons in the substantia nigra pars compacta (SNpc) compared with saline treatment.

85 volume of the anterior, posterior, and whole SNpc correlated with Unified Parkinson's Disease Rating

86 lin or the ghrelin receptor (GHSR) increased SNpc DA cell loss and lowered striatal dopamine levels a

87 Exogenous ghrelin administration decreased SNpc DA cell loss and restricted striatal dopamine loss

88 uce overt motor abnormalities or substantial SNpc DA neuron loss.

89 mice defective in NADPH-oxidase exhibit less SNpc DA neuronal loss and protein oxidation than their W

90 re, the localization of ERbeta and IGF-1R on SNpc DA neurons and astrocytes suggests a modulatory rol

91 uced spread of aggregated alpha-syn, loss of SNpc DA neurons and increased neuroinflammation.

92 LRRK2 G2019S on the function and survival of SNpc DA neurons are poorly understood.

93 gest that ALDH1A1 protects subpopulations of SNpc DA neurons by preventing the accumulation of dopami

94 the theory that D-amphetamine inhibition of SNPC DA neurons is dependent upon neuronal negative feed

95 and protein were similarly decreased in the SNpc DA neurons of aged G2019S mice.

96 F-1R mRNA and revealed that almost all TH-ir SNpc DA neurons were immunoreactive for IGF-1R, respecti

97 binds to SNpc cells, electrically activates SNpc DA neurons, increases tyrosine hydroxylase mRNA and

98 ial mechanisms by which LRRK2 G2019S acts in SNpc DA neurons, resulting in downregulation of its down

99 nucleus (CN), the major projection area for SNPC DA neurons.

100 ase-immunoreactive (TH-ir) SN pars compacta (SNpc) DA neurons are immunoreactive for estrogen recepto

101 In rodent SNpc, DA neurons can be divided into two subpopulations

102 DANs) in the substantia nigra pars compacta (SNpc), decrease of dopamine (DA) transmitter, and increa

103 on of DNs in substantia nigra pars compacta (SNpc), decreased striatal dopamine levels and swellings

104 thening the apoptotic nature of the observed SNpc developmental cell death, we demonstrate that overe

105 in the SNpc and that its ablation attenuates SNpc developmental neuronal apoptosis.

106 s within the substantia nigra pars compacta (SNpc) display a differential vulnerability to loss in Pa

107 minergic terminal density and modest loss of SNpc dopamine neurons after eight weeks, corresponding t

108 ation of EUK-189 decreases paraquat-mediated SNpc dopaminergic neuronal cell death in vivo.

109 s as to the occurrence of this phenomenon in SNpc dopaminergic neurons in the developing mouse.

110 tosis and results in a lower number of adult SNpc dopaminergic neurons.

111 ic synapses on VTA dopaminergic neurons than SNpc dopaminergic neurons.

112 s and cholinergic interneurons compared with SNpc dopaminergic neurons.

113 of midbrain substantia nigra pars compacta (SNpc) dopaminergic (DA) neurons contributes to the main

114 by a loss of substantia nigra pars compacta (SNpc) dopaminergic (DA) neurons, and can be modeled by t

115 r expression in the resistant neurons of the SNpc dorsal tier.

116 DA lesion differed between regions, with the SNpc exhibiting the greatest loss of neurons (46%), but

117 cated in the substantia nigra pars compacta (SNpc), expression of monoamines and indolamines in brain

118 ventral tier substantia nigra pars compacta (SNpc) failed to demonstrate a preponderance of a particu

119 on were similar to those required to inhibit SNPC firing.

120 e other contained a phosphorylcholine (DiC(6)SNPC) headgroup.

121 loss in the substantia nigra pars compacta (SNpc) in Parkinson disease (PD) is not uniform, as dopam

122 Stimulation of the SNpc increased gastric tone and motility via activation

123 pic glutamate receptor agonist, NMDA, in the SNpc increased proximal colonic motility and tone, as me

124 elective loss of dopaminergic neurons in the SNpc, indicating that LRRK DKO mice are unique models fo

125 s within the substantia nigra pars compacta (SNpc) is a defining pathological hallmark of Parkinson's

126 s within the substantia nigra pars compacta (SNpc), locus coeruleus, and ventral tegmental area in Pa

127 elated volumes of the anterior and posterior SNpc, locus coeruleus, and ventral tegmental area were d

128 e in PD was most pronounced in the posterior SNpc (median, -83%; P < .001), followed by the anterior

129 nes and indolamines in brain, alterations in SNpc microglia number and morphology, and expression of

130 ouse strains exhibit dramatic differences in SNpc neuron survival, ranging from 63% cell loss in C57B

131 mb akinesia, striatal denervation or loss of SNpc neuron, nor did STN DBS elevate p-rpS6 levels furth

132 ptomes of ~100 laser captured microdissected SNpc neurons from each tier from 7 healthy controls.

133 of morphologic techniques, we show that many SNpc neurons fulfill the criteria for apoptosis and that

134 The surviving SNpc neurons in LRRK DKO mice at 25 months of age accumu

135 en mitochondria and presynaptic terminals of SNpc neurons in PD brains vs. DBS-treated brains, DBS tr

136 The majority of SNpc neurons undergoing apoptotic-like cell death did no

137 One case had no LB-containing SNpc neurons undergoing apoptotic-like cell death.

138 Three cases demonstrated that SNpc neurons with LBs in the perikarya had the same prop

139 r apoptotic-like changes were more common in SNpc neurons with somal LBs compared to those without so

140 same proportion of apoptotic-like changes as SNpc neurons without somal LBs.

141 rylation of ribosomal protein S6 (p-rpS6) in SNpc neurons, a readout of trkB activation.

142 doses above those inhibiting firing rates of SNPC neurons.

143 part, due to a neuromodulatory effect on the SNpc neurons.

144 ting neurons in the DMV received inputs from SNpc neurons.

145 ctivation of substantia nigra pars compacta (SNpc) neurons alleviates parkinsonism in acute PD animal

146 Substantia nigra pars compacta (SNpc) neurons are connected to the dorsal motor nucleus

147 zyme during inflammation, is up-regulated in SNpc of human PD and MPTP mice.

148 some of the neuronal death occurring in the SNpc of Lewy body-associated disorders resembles apoptos

149 dent increases of autophagic vacuoles in the SNpc of LRRK(-/-) mice before the onset of DA neuron los

150 a morphology of apoptosis does occur in the SNpc of mice and that this process plays a critical role

151 peroxidation and DA neurodegeneration in the SNpc of mice breathing 21% oxygen, but not in those brea

152 ve reactive microgliosis was observed in the SNpc of MPTP-lesioned IL-6 (+/+) mice.

153 ylase-positive and total cell numbers in the SNpc of MPTP-lesioned mice, even though this did not inc

154 kin expression in cultured cells; and in the SNpc of PD patients, Parkin levels are reduced in a subs

155 Consistently, SNpc of postmortem PD patients shows a significant popul

156 were evident for dopaminergic neurons in the SNpc of Wistar vs. Sprague-Dawley rat strains.

157 otein in the substantia nigra pars compacta (SNpc) of human PD patients that correlated significantly

158 urons of the substantia nigra pars compacta (SNpc) of human PD patients.

159 ction in the substantia nigra pars compacta (SNpc) of mice and rats.

160 ccurs in the substantia nigra pars compacta (SNpc) of patients with Parkinson's disease and other Lew

161 shown in the substantia nigra pars compacta (SNpc) of PD models when there has been a decrease in tyr

162 S10 into the substantia nigra pars compacta (SNpc) of rats reduced microgliosis and protected against

163 (PD), in the substantia nigra par compacta (SNpc) of the brain in a PD mouse model.

164 effect on the firing rates of DA neurons in SNPC, on type II anterior CN neurons, or on the effects

165 to the somata of dopaminergic neurons in the SNpc or dorsal striatal cholinergic interneurons.

166 ephalic DA progenitors were grafted into the SNpc or into the striatum of SNpc or striatum of alpha-s

167 rafted into the SNpc or into the striatum of SNpc or striatum of alpha-syn injected mice, respectivel

168 irus2/9-human alpha-syn A53T into either the SNpc or the striatum of C57BL/6 mice.

169 gene expression variation in human and mouse SNpc populations strongly argues for the need of human-f

170 the ventral substantia nigra pars compacta (SNpc) preferentially degenerate in Parkinson's disease (

171 n dopaminergic neurons (mDAs) in the VTA and SNpc project to different regions and form distinct circ

172 urons in the substantia nigra pars compacta (SNpc) remains to be answered.

173 Quantification of DA neurons in the SNpc show that mice allowed to run unrestricted for 1 or

174 Quantification of DA neurons in the SNpc show that mice whose running was restricted lost si

175 proximal colon and of anterograde tracers in SNpc showed that bilaterally labelled colonic-projecting

176 n control in substantia nigra pars compacta (SNpc) somata and neurites but unchanged in ventral tegme

177 y a reduction of dopaminergic neurons in the SNpc, striatal neuritic density was increased upon myelo

178 o either the substantia nigra pars compacta (SNpc), the lateral ventricle (LV) or the striatum (or co

179 significant reduction of DANs (~35%) in the SNpc, the tyrosine hydroxylase protein level in the stri

180 The genes higher in the dorsal/resistant SNpc tier neurons displayed coordinated patterns of expr

181 d for genes higher in the ventral/vulnerable SNpc tier.

182 rentially expressed genes (DEGs) between the SNpc tiers.

183 connects the substantia nigra pars compacta (SNpc) to neurons of the dorsal motor nucleus of the vagu

184 ion of nigro-vagal nerve terminals following SNpc transfection with pAAV-hSyn-hM4D(Gi)-mCherry decrea

185 urons in the substantia nigra pars compacta (SNpc) undergo natural cell death during development in r

186 ions and spatially localized each within the SNpc using Slide-seq.

187 that the number of apoptotic neurons in the SNpc vary in a time-dependent manner from postnatal day

188 cells in the substantia nigra pars compacta (SNpc), ventral tegmental area (VTA), and retrorubral fie

189 entially affects dopaminergic neurons in the SNpc, VTA, and RRF; however, the resulting changes in nu

190 nd spatially confined to the ventral tier of SNpc, was highly susceptible to loss in PD and showed th

191 ng CR in the substantia nigra pars compacta (SNpc) were relatively spared compared to those that did

192 Binding of DiC(6)SNPC with 2.0 mM Triton X-100 showed positive cooperativ

193 Upon transfection of SNpc with pAAV-hSyn-hM3D(Gq)-mCherry, chemogenetic activ