ライフサイエンスコーパス: mature neuron

1 stem/progenitor cell and from progenitor to mature neuron.

2 , spanning nearly the entire axonal shaft of mature neurons.

3 oride-permeable ionotropic GABAA receptor in mature neurons.

4 cline of intrinsic axon growth capability in mature neurons.

5 xpression and differentiated these NSCs into mature neurons.

6 ocampal neural progenitors into functionally mature neurons.

7 esting a postsynaptic role for mRNAs in more mature neurons.

8 lineage during embryonic development and in mature neurons.

9 ent structural change of dendritic spines in mature neurons.

10 ppocampus, the vast majority of which become mature neurons.

11 s in synaptic transmission and plasticity of mature neurons.

12 d responses than did DAMGO at native MOPr in mature neurons.

13 lopment and to programmed gene expression in mature neurons.

14 e brain where it is expressed selectively in mature neurons.

15 e morphogenesis and long-term maintenance of mature neurons.

16 nction as the predominant MT deacetylases in mature neurons.

17 axonal transport, a process that is used by mature neurons.

18 e and results in the ectopic localization of mature neurons.

19 ablation of neurogenesis increased EPSCs in mature neurons.

20 implicated as sensors of diverse stimuli in mature neurons.

21 are any differences between the immature and mature neurons.

22 s, diminished in newborn neurons, and low in mature neurons.

23 h major differences between the immature and mature neurons.

24 h becomes pathological upon AICD increase in mature neurons.

25 d neuronal activity or sensory experience in mature neurons.

26 ed Zn(2+) potentiation were also recorded in mature neurons.

27 The EdU-positive cells differentiated into mature neurons.

28 viability compared with glial cells and more mature neurons.

29 and organelles, is essential for survival of mature neurons.

30 ying some postsynaptic signaling cascades in mature neurons.

31 ates diverse processes that are essential in mature neurons.

32 ma-mediated clearance of SINV infection from mature neurons.

33 AP150 decreased dendritic spine area only in mature neurons.

34 nses; it also possesses paracrine effects on mature neurons.

35 s and show enhanced plasticity compared with mature neurons.

36 acquiring markers of neuronal precursors and mature neurons.

37 enic mice with reduced TGF-beta signaling in mature neurons.

38 nover or even after acute, selective loss of mature neurons.

39 duce Apaf-1 expression in developing but not mature neurons.

40 ing cellular communication in developing and mature neurons.

41 F mRNA was restricted to cells identified as mature neurons.

42 n the differentiation of progenitor cells to mature neurons.

43 eveloping neurons and repressed chromatin in mature neurons.

44 c currents within 4-6 h when cocultured with mature neurons.

45 A(A) receptors, causing hyperpolarization of mature neurons.

46 ferentiation, controls secretory capacity in mature neurons.

47 is an important event in both developing and mature neurons.

48 r repetitive stimulation in immature but not mature neurons.

49 and a subset of neural progenitor cells and mature neurons.

50 ular events involved in virus clearance from mature neurons.

51 ripotent ES cells, multipotent NS cells, and mature neurons.

52 mediated noncytolytic clearance of SINV from mature neurons.

53 ytosolic NOS contributes to NMDA toxicity in mature neurons.

54 defines a gene set subject to plasticity in mature neurons.

55 w they integrate into an existing network of mature neurons.

56 s-GRFs endow NMDARs with functions unique to mature neurons.

57 tic inhibitors, which is a characteristic of mature neurons.

58 sterior axis by the selective elimination of mature neurons.

59 ed the in vitro differentiation of NSCs into mature neurons.

60 late transcription during the development of mature neurons.

61 datory for spine stability and plasticity in mature neurons.

62 otent stem cells to neuronal progenitors and mature neurons.

63 le of Stx1 for maintenance of developing and mature neurons.

64 broadly responsive to afferent activity than mature neurons.

65 essed in a largely non-overlapping manner by mature neurons.

66 nd expression is almost completely absent in mature neurons.

67 by enhancing microtubule sliding in injured mature neurons.

68 nd the importance of chromatin regulation in mature neurons.

69 to a short lasting increase of the kinase in mature neurons.

70 SPCs and their progeny would result in fewer mature neurons.

71 is a chromatin regulator highly expressed in mature neurons.

72 appearing as a novel epigenomic signature in mature neurons.

73 alcium influx through feedback regulation in mature neurons.

74 with subcellular localization indicative of mature neurons.

75 al neurons but presumably different roles in mature neurons.

76 ew enhancers bound by clusters of Onecut1 in maturing neurons.

77 y before birth, both in progenitor cells and maturing neurons.

78 e into robust typological distinctions among maturing neurons.

79 transfect single autaptic neurons as well as mature neurons (15-82 days in vitro) for gene functional

80 In contrast, in mature neurons a decrease in HDAC2 levels alone was suff

81 integrate in close proximity to the soma of mature neurons, a behavior that may explain the emergenc

82 ited in their capacity to differentiate into mature neurons, a phenotype akin to animals lacking p27.

83 ssion in the brain, where the loss of PTB in maturing neurons allows the synthesis of nPTB in these c

84 Knocking out Sez6 in a small subset of mature neurons also prevented the structural postsynapti

85 e cells; however, these cells generated less mature neurons, although they did produce astrocytes and

86 In mature neurons AMPA receptors cluster at excitatory syna

87 s differentiation of neuronal progenitors to mature neurons, an activity mediated in part by the PPAR

88 undamental for maintenance of developing and mature neurons and also for vesicle docking and neurotra

89 y generated cells expressed markers for more mature neurons and astrocytes.

90 adly tuned young neurons and highly specific mature neurons and describe how the fidelity of memories

91 r nerve injury, the MGE cells developed into mature neurons and exhibited firing patterns characteris

92 also expressed in adult tissues, notably in mature neurons and glia in the brain, where their roles

93 enic differentiation, with the generation of mature neurons and glia over 4 weeks in vitro, and 20 we

94 ogenitors and, ultimately, the generation of mature neurons and glia.

95 tential to neural progenitors and further to mature neurons and glia.

96 ural progenitors as well as for immature and mature neurons and glial cells.

97 2+) influx in both spontaneously oscillating mature neurons and in non-oscillatory immature neurons.

98 2 is a transcriptional repressor elevated in mature neurons and is predicted to be required for neuro

99 e regulation mechanism of ER organization in mature neurons and its disruption causes previously unde

100 sion, the accumulation of gamma-tubulin-2 in mature neurons and neuroblastoma cells during oxidative

101 l net (PNN), a specialized ECM that envelops mature neurons and restricts synapse formation.

102 tic activity drives DNA demethylation within mature neurons and suppresses basal synaptic function.

103 of the retinorecipient layers of the SC into mature neurons and that loss of Gata2 arrests them at an

104 diminished intrinsic axon growth capacity of mature neurons and the hostile extrinsic environment com

105 ls of virus replication between immature and mature neurons and the molecular events involved in viru

106 ntracellular chloride concentration found in mature neurons and thereby establishes the driving force

107 of neuronal precursors to differentiate into mature neurons and to excessive cell death.

108 licating efforts to study O-GlcNAcylation in mature neurons and to understand its roles in disease.

109 sed in neural progenitor cells, immature and matured neurons and glial cells.

110 lurane significantly decreased the number of maturing neurons and increased the number of astrocytes

111 irus replication is an intrinsic property of maturing neurons and that the CSM14.1 cell line is a con

112 ls are capable of differentiation, some into mature neurons, and could potentially be of value in the

113 the early neuronal marker, NeuN to identify mature neurons, and glial fibrillary acidic protein to i

114 tivation of genes that are only expressed in mature neurons, and is now found to protect the genome o

115 creased nestin expressing neural stem cells, mature neurons, and oligodendrocytes by 33, 75, and 30%,

116 on neuron projections, at the presynapse in mature neurons, and on the soma of immature neurons in t

117 several proteins that distinguish them from mature neurons, and the promoters for these genes have b

118 immature neurons with a slight effect on the mature neurons; and 5) delta-opioid receptor activation

119 In some areas of the OE, mature neurons are absent, or sparse, although those sam

120 dual human neural precursor cells (NPC) into mature neurons are currently not fully understood.

121 Terminally differentiated, mature neurons are essential cells that are not easily r

122 Not knowing which mature neurons are made by specific INPs, however, conce

123 r events required for robust regeneration of mature neurons are not fully understood, particularly in

124 Because mature neurons are not readily regenerated, recovery fro

125 ntiation and development and the activity of mature neurons are significantly determined and regulate

126 short- and long-term synaptic plasticity in mature neurons as well as for the survival of cortical n

127 We further show that AICD increase in mature neurons, as reported in AD, alters synaptic NMDAR

128 ed iNSCs differentiate into several types of mature neurons, as well as astrocytes and oligodendrocyt

129 SynI relocation to extrasynaptic regions of mature neurons, as well as SynI dispersion from synaptic

130 ally illustrate how the apoptotic pathway in mature neurons becomes increasingly restricted by a nove

131 pressed in multipotent neural precursors and mature neurons but is not detectable in glia.

132 ion of KLF4 fail to migrate and develop into mature neurons but, rather, form cells with a glial iden

133 wn for mediating neurotransmitter release in mature neurons, but its potential role in axonal guidanc

134 fraction of dendritic regions in relatively mature neurons, but this structure develops slower and f

135 ndrocyte viability, but reduced viability of mature neurons by 30%, and reduced survival of Dcx(+) ce

136 hat Nfasc186 optimizes communication between mature neurons by anchoring the key elements of the adul

137 also diminished the dendritic complexity of mature neurons by decreasing the levels of pAKT and pGSK

138 causes the death of immature neurons, while mature neurons can often survive infection.

139 s in the environment, dendrites from certain mature neurons can undergo large-scale morphologic remod

140 Indeed, reducing the expression of MyH7B in mature neurons caused profound alterations to dendritic

141 Constitutive activation of Rho in mature neurons causes dendritic spine loss and dendritic

142 siveness to injury-induced growth factors in mature neurons contributes significantly to regeneration

143 as developmentally regulated specifically in maturing neurons, correlating with HBII-85 nucleolar acc

144 Herein, we provide evidence that mature neurons cultured in physiological KCl develop spo

145 In mature neurons, dendritic vesicles that entered the base

146 work, we describe a presynaptic phenotype in mature neurons derived from MAP1B knockout (MAP1B KO) mi

147 In mature neurons, DLK is present in the synapse and intera

148 A(A) receptor deficit induced selectively in mature neurons during adolescence lacked neurogenic and

149 id decarboxylase and tyrosine hydroxylase in mature neurons during early and late differentiation of

150 tion of the appropriate types and numbers of mature neurons during the development of the spinal cord

151 l colocalization of DCX with markers of more mature neurons, e.g., human neuronal protein C and D (Hu

152 ms to be required for proper development: in maturing neurons, ectopic Nrf2 expression inhibits neuri

153 We find that, in mature neurons, EphB2 expression levels regulate the amo

154 ad a tendency to increase the density in the mature neurons, except for taurine; 4) under hypoxia, al

155 Mature neurons express a large number of distinct miRNAs

156 Mature neurons express MAP1B, and its deficiency does no

157 of neuronal progenitors and nascent, but not mature, neurons express INSM1.

158 Most mature neurons expressed only one of the ~1000 odorant r

159 cation and expression of secreted factors in mature neurons for extrinsic modulation of neurogenesis

160 MAP kinase cascade is required to switch the mature neuron from an aplastic state to a state capable

161 dult neurogenesis, the process of generating mature neurons from adult neural stem cells, proceeds co

162 dult neurogenesis, the process of generating mature neurons from neuronal progenitor cells, makes cri

163 s and immature neurons, and DeltaOMP-eGFP(+) mature neurons from normal adult mice.

164 factors decrease over development to protect mature neurons from stressful insults, making them less

165 ical evidence that embryonic origin dictates mature neuron function within cranial sensory ganglia: s

166 by decreased expression of genes involved in mature neuron function, along with increased expression

167 Here we show that relatively mature neurons generated from neurospheres derived from

168 n OE biopsy express markers for immature and mature neurons, grossly recapitulating neuronal differen

169 effect of PI3K on dendrites was lost in more mature neurons (>14 d in vitro).

170 isting spines and the amplitude of mEPSCs in mature neurons (>21 d in vitro) within 24 h after transf

171 However, in more mature neurons (>DIV17) application of NMDA produces con

172 ological development of synaptic inputs onto maturing neurons has restricted our understanding of how

173 Mature neurons have diminished intrinsic regenerative ca

174 dex during neurogenesis and the long life of mature neurons highlight the need for efficient cellular

175 In mature neurons, however, presynaptic boutons are mostly

176 SAP102 is highly expressed in both young and mature neurons; however, little is known about its local

177 ignaling, which is in sharp contrast to most mature neurons hyperpolarized by GABA.

178 AAV r3.45 was more selective for NSCs than mature neurons in a human embryonic stem cell-derived cu

179 urogenesis modifies synaptic transmission to mature neurons in a manner consistent with a redistribut

180 tic cell counts in development and counts of mature neurons in adulthood; the molecular mechanisms of

181 ice) that expressed high levels of EC-SOD in mature neurons in an otherwise EC-SOD-deficient environm

182 we provide evidence that P7C3 also protects mature neurons in brain regions outside of the hippocamp

183 sis confirmed no significant increase of new mature neurons in hippocampi of TgCRND8 compared with WT

184 in slices paradoxically generates spiking of mature neurons in the absence of immature neuron spiking

185 the poor intrinsic regenerative capacity in mature neurons in the adult mammalian central nervous sy

186 Mature neurons in the adult peripheral nervous system ca

187 eural stem cells (NSCs), astrocytes, or even mature neurons in the brains of mice can give rise to ma

188 ls (NPCs), fewer immature neurons, and fewer mature neurons in the dentate gyrus of the hippocampus o

189 hem a functional role that is different from mature neurons in the DG circuit, a distinction that pot

190 st to neurons in the central nervous system, mature neurons in the mammalian peripheral nervous syste

191 ent study, we instead focus on plasticity in mature neurons in the neocortex of adult animals.

192 After 4 weeks, the GFAP lineage generated mature neurons in the olfactory bulb (OB), DG, and, stri

193 ental continuum that results in depletion of mature neurons in the olfactory bulb.

194 proliferation, total cell numbers, number of mature neurons in the olfactory epithelium, and reactive

195 iation of multipotent neural precursors into mature neurons in vitro and that PrP(c) levels positivel

196 However, generation of physiologically mature neurons in vitro remains problematic.

197 in the progression of neuronal precursors to mature neurons in vivo.

198 study the effects of cell cycle re-entry on mature neurons in vivo.

199 nd anatomically significantly different than mature neurons in vivo.

200 related activity patterns among ensembles of maturing neurons in the lateral geniculate nucleus (LGN)

201 At present, the break repair capabilities of mature neurons, in general, and rod cells, in particular

202 annels, the opposite direction compared with mature neurons, in which GABA(A) receptor activation is

203 loy the postsynaptic mechanism, whereas more mature neurons increase their strength through the presy

204 Dendritic spine density of mature neurons increased and synaptic plasticity improve

205 verexpression of human AKAP79 in immature or mature neurons increased the number of dendritic filopod

206 An alternative hypothesis posits that maturing neurons "indirectly" contribute to memory encod

207 ique properties and structural plasticity of mature neurons induced by new-neuron integration.

208 l neurons is required for the integration of maturing neurons into the coordinated CPG network.

209 The mechanisms by which injury unlocks mature neurons' intrinsic axonal growth competence are n

210 in, not only during development, but also in mature neurons involved in long-term memory.

211 s define how the stable MT cytoskeleton of a mature neuron is converted into the dynamically growing

212 diminished intrinsic regenerative ability of mature neurons is a major contributor to regeneration fa

213 Instead, NF-kappaB in mature neurons is activated by stimuli that induce deman

214 The mechanism by which the number of mature neurons is determined in the central nervous syst

215 Chloride extrusion in mature neurons is largely mediated by the neuron-specifi

216 ession from neural precursor cells (NPCs) to mature neurons is tightly controlled by coordinate cell-

217 and neurogenesis; however, their function in mature neurons is unknown.

218 -associated protein 2c (Map-2c), a marker of mature neurons, is nearly absent in Cdk5(-/-) cells that

219 In mature neurons, it is localized to dendritic spines, but

220 mature neurons that gradually developed into mature neurons, leading to a late increase in the volume

221 How transient activation of mature neurons leads to long-lasting modulation of adult

222 riple-label immunofluorescence for BrdU, the mature neuron marker neuronal nuclear antigen, and the a

223 new Cr(+) or GABA(+) cells colabeled with a mature neuron marker, NeuN or chondroitin sulfate antibo

224 an Amplex Red cholesterol assay showed that mature neuron membrane cholesterol levels were significa

225 Mature neurons (MNs), neural progenitor cells (NPCs) and

226 nd low in newly generated neurons (NGNs) and mature neurons (MNs).

227 activation (Iba-1) increased while index of mature neurons (NeuN) significantly decreased in all bra

228 this induction is prolonged, whereas in more mature neurons, NMDA receptor stimulation induces a prot

229 In turn, overexpressing PRG5 in mature neurons not only increased Homer-positive spine n

230 In mature neurons, NR2B is coupled to inhibition rather tha

231 or neurons, but that it is also a feature of mature neurons of both the main and accessory olfactory

232 robust, and reproducible method to generate mature neurons of many different subtypes from multiple

233 ations in the organization of newly born and mature neurons of the dentate gyrus.

234 rences in gene expression as compared to the mature neurons of the normal epithelium.

235 nd medial amygdala differentiate into either mature neurons or astrocytes.

236 lations of neuroglial stem/progenitor cells, mature neurons or epithelial-mesenchymal cells.

237 ponses of immature LGN neurons compared with mature neurons, our results show that correlated activit

238 potential for the aged stem cell to yield a mature neuron persisted at the same rate as that observe

239 in contrast to astrocytes or young neurons, maturing neurons possess negligible Nrf2-dependent antio

240 Corresponding analysis of mature neurons predicted minimal change in neuronal exci

241 ganizer protein Satb1 is highly expressed in mature neurons, primarily in the cerebral cortex, dentat

242 In mature neurons, Ptch and Smo are concentrated in dendrit

243 sion is only detectable in subpopulations of mature neurons, raising the question of how these inhibi

244 thermore, decreasing membrane cholesterol in mature neurons reduced their susceptibility to Abeta-dep

245 regulating the cell cycle and cell death in mature neurons remains elusive.

246 , the molecular mechanism how Notch works in mature neurons remains uncertain.

247 llowing downregulation of programming TFs in maturing neurons remains unknown.

248 Rather, Apaf-1 up-regulation in mature neurons requires both chromatin derepression and

249 As progenitors differentiate into mature neurons, REST leaves miR-124a gene loci, and nonn

250 Lowering ARF6 activity in mature neurons restores anterograde integrin flow, allow

251 Also, mature neurons restrict apoptosis but remain permissive

252 at decreasing membrane cholesterol levels in mature neurons resulted in a significant reduction of th

253 Furthermore, knockdown of ZNF804A in mature neurons resulted in the loss of dendritic spine d

254 dicate that abrogation of Cdk5 expression in mature neurons results in a viable mouse model that offe

255 However, after DNA damage, mature neurons resynthesize Apaf-1 through the cell cycl

256 Morphological analysis of mature neurons revealed significantly altered neurite le

257 Why mature neurons should be particularly sensitive to such

258 ort membrane organelles is not diminished in mature neurons, suggesting that microtubule sliding is r

259 concert with reduced synaptic inhibition of mature neurons, suggesting that the local circuitry coor

260 contain disparate and fluctuating numbers of mature neurons, tactics employed by neuronal networks to

261 In mature neurons, TBB reduces the axodendritic polarity of

262 he proliferating crest-derived precursors of mature neurons that are not catecholaminergic and, thus,

263 An interesting secondary depolarization in mature neurons that followed an initial hyperpolarizatio

264 Mature neurons that have experienced the overexpression

265 esults identify a unique strategy evolved by maturing neurons that uses a single microRNA to inhibit

266 express EpoR at higher levels compared with mature neurons; that Epo stimulates proliferation of emb

267 In mature neurons the PHR proteins also regulate axon degen

268 In mature neurons, the number of synapses is determined by

269 endritogenesis-associated gene expression in maturing neurons through delayed binding of NFI proteins

270 results demonstrate that CAR is expressed by mature neurons throughout the brain.

271 In addition, selective KO of Cdk5 from mature neurons throughout the hippocampus reduced the nu

272 nance of transmembrane chloride potential in mature neurons; thus KCC2 activity is critical for hyper

273 isoforms expressed during development allows mature neurons to generate afterdischarges that are requ

274 tatory and inhibitory receptor activation in mature neurons to provide an activity-dependent scaling

275 ion of NR2B-containing NMDARs at synapses of mature neurons; triple EphB knock-out mice lacking EphB1

276 and mature neurons under normoxia and in the mature neurons under hypoxic condition.

277 ases (Cdks) are inappropriately activated in mature neurons under ischemic stress conditions.

278 GlyRalpha1 density in both the immature and mature neurons under normoxia and in the mature neurons

279 ed, recovery from encephalitis suggests that mature neurons utilize unique antiviral mechanisms to bl

280 f neuronal progenitor cells and a deficit in mature neurons versus wild-type animals.

281 h unoperated controls (n = 7), the number of mature neurons was about 70% higher in the paralaminar n

282 Localization of gamma-tubulin-1 in mature neurons was confirmed by immunohistochemistry and

283 The molecular repertoire of mature neurons was sculpted by SOC-related up- and down-

284 ese mechanistic elements are widely found in mature neurons, we expect them to apply broadly to elect

285 es of immature interneurons to those of more mature neurons, we identified genes important for human

286 As Fmrp is also enriched in mature neurons, we investigated the function of Fmrp exp

287 Our results revealed that mature neurons were more susceptible to Abeta-induced ca

288 Because mature neurons were not evident at 6 wk, we examined tis

289 points, immature neuroblasts, and eventually mature neurons, were infected as determined by expressio

290 o the previously described role of CASPR2 in mature neurons, where CASPR2 organizes nodal microdomain

291 izes strongly to the axon initial segment in mature neurons, where it plays a role in assembling and

292 naptic currents (EPSCs) and spine density in mature neurons, whereas genetic ablation of neurogenesis

293 stimulates axon formation and elongation of mature neurons whether in presence or absence of inhibit

294 and Ca2+-induced E(Cl) shifts were larger in mature neurons, which express the K-Cl cotransporter KCC

295 of Ser(473)-Akt species to PTEN deletion in mature neurons, which suggests inherent differences in t

296 ated into the rat cerebellum developing into mature neurons while retaining mouse-specific morphometr

297 e combined silencing of endogenous PSD-95 in mature neurons with heterologous expression of specific

298 additional week of differentiation produces mature neurons with many features of cortical pyramidal

299 transmitters of the incoming frequency, and mature neurons, with narrow frequency response, that are

300 del of hippocampal neurogenesis and protects mature neurons within the substantia nigra in a mouse mo