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1 t brain, little is known about their role in mature neurons.
2  culture derived a mixture of Tbr1 and Ctip2 mature neurons.
3 nd expression is almost completely absent in mature neurons.
4  by enhancing microtubule sliding in injured mature neurons.
5 nd the importance of chromatin regulation in mature neurons.
6  adult mammalian brain is mainly composed of mature neurons.
7 to a short lasting increase of the kinase in mature neurons.
8 SPCs and their progeny would result in fewer mature neurons.
9 is a chromatin regulator highly expressed in mature neurons.
10 appearing as a novel epigenomic signature in mature neurons.
11 alcium influx through feedback regulation in mature neurons.
12 al neurons but presumably different roles in mature neurons.
13 cline of intrinsic axon growth capability in mature neurons.
14 xpression and differentiated these NSCs into mature neurons.
15  which were subsequently differentiated into mature neurons.
16 esting a postsynaptic role for mRNAs in more mature neurons.
17  lineage during embryonic development and in mature neurons.
18 ent structural change of dendritic spines in mature neurons.
19 ppocampus, the vast majority of which become mature neurons.
20 is as well as maintain inhibitory control of mature neurons.
21 s in synaptic transmission and plasticity of mature neurons.
22 d responses than did DAMGO at native MOPr in mature neurons.
23 e brain where it is expressed selectively in mature neurons.
24 e morphogenesis and long-term maintenance of mature neurons.
25 nction as the predominant MT deacetylases in mature neurons.
26  axonal transport, a process that is used by mature neurons.
27 e and results in the ectopic localization of mature neurons.
28  implicated as sensors of diverse stimuli in mature neurons.
29 are any differences between the immature and mature neurons.
30 s, diminished in newborn neurons, and low in mature neurons.
31 h major differences between the immature and mature neurons.
32 ties of developing neurons, but not those of mature neurons.
33 d neuronal activity or sensory experience in mature neurons.
34 ed Zn(2+) potentiation were also recorded in mature neurons.
35   The EdU-positive cells differentiated into mature neurons.
36 viability compared with glial cells and more mature neurons.
37 and organelles, is essential for survival of mature neurons.
38 bditis elegans DIP-2 maintains morphology of mature neurons.
39 ying some postsynaptic signaling cascades in mature neurons.
40 ma-mediated clearance of SINV infection from mature neurons.
41 AP150 decreased dendritic spine area only in mature neurons.
42 nses; it also possesses paracrine effects on mature neurons.
43 s and show enhanced plasticity compared with mature neurons.
44 acquiring markers of neuronal precursors and mature neurons.
45 nover or even after acute, selective loss of mature neurons.
46 duce Apaf-1 expression in developing but not mature neurons.
47 ing cellular communication in developing and mature neurons.
48 egulation of translation during infection of mature neurons.
49 n the differentiation of progenitor cells to mature neurons.
50 eveloping neurons and repressed chromatin in mature neurons.
51 c currents within 4-6 h when cocultured with mature neurons.
52 A(A) receptors, causing hyperpolarization of mature neurons.
53 ferentiation, controls secretory capacity in mature neurons.
54 is an important event in both developing and mature neurons.
55 f antiapoptotic and innate immune factors in mature neurons.
56 x of mice, LMO3-iPS-NPCs differentiated into mature neurons.
57  physiological changes to become functional, mature neurons.
58 , spanning nearly the entire axonal shaft of mature neurons.
59 late transcription during the development of mature neurons.
60  with subcellular localization indicative of mature neurons.
61 oride-permeable ionotropic GABAA receptor in mature neurons.
62 ocampal neural progenitors into functionally mature neurons.
63 lopment and to programmed gene expression in mature neurons.
64  ablation of neurogenesis increased EPSCs in mature neurons.
65 h becomes pathological upon AICD increase in mature neurons.
66 ates diverse processes that are essential in mature neurons.
67 enic mice with reduced TGF-beta signaling in mature neurons.
68 F mRNA was restricted to cells identified as mature neurons.
69 ed the in vitro differentiation of NSCs into mature neurons.
70 datory for spine stability and plasticity in mature neurons.
71 otent stem cells to neuronal progenitors and mature neurons.
72 le of Stx1 for maintenance of developing and mature neurons.
73 broadly responsive to afferent activity than mature neurons.
74 essed in a largely non-overlapping manner by mature neurons.
75 e into robust typological distinctions among maturing neurons.
76 ew enhancers bound by clusters of Onecut1 in maturing neurons.
77 y before birth, both in progenitor cells and maturing neurons.
78 transfect single autaptic neurons as well as mature neurons (15-82 days in vitro) for gene functional
79                              In contrast, in mature neurons a decrease in HDAC2 levels alone was suff
80  integrate in close proximity to the soma of mature neurons, a behavior that may explain the emergenc
81 ited in their capacity to differentiate into mature neurons, a phenotype akin to animals lacking p27.
82 ssion in the brain, where the loss of PTB in maturing neurons allows the synthesis of nPTB in these c
83       Knocking out Sez6 in a small subset of mature neurons also prevented the structural postsynapti
84 e cells; however, these cells generated less mature neurons, although they did produce astrocytes and
85                                           In mature neurons AMPA receptors cluster at excitatory syna
86 s differentiation of neuronal progenitors to mature neurons, an activity mediated in part by the PPAR
87 undamental for maintenance of developing and mature neurons and also for vesicle docking and neurotra
88 adly tuned young neurons and highly specific mature neurons and describe how the fidelity of memories
89 r nerve injury, the MGE cells developed into mature neurons and exhibited firing patterns characteris
90  also expressed in adult tissues, notably in mature neurons and glia in the brain, where their roles
91 enic differentiation, with the generation of mature neurons and glia over 4 weeks in vitro, and 20 we
92 ogenitors and, ultimately, the generation of mature neurons and glia.
93 tential to neural progenitors and further to mature neurons and glia.
94 2 is a transcriptional repressor elevated in mature neurons and is predicted to be required for neuro
95 e regulation mechanism of ER organization in mature neurons and its disruption causes previously unde
96 ng cell line that can be differentiated into mature neurons and latently infected with HSV-1.
97 sion, the accumulation of gamma-tubulin-2 in mature neurons and neuroblastoma cells during oxidative
98 lt mice, we observed that TET3 is present in mature neurons and oligodendrocytes but is absent in ast
99 l net (PNN), a specialized ECM that envelops mature neurons and restricts synapse formation.
100 tic activity drives DNA demethylation within mature neurons and suppresses basal synaptic function.
101 of the retinorecipient layers of the SC into mature neurons and that loss of Gata2 arrests them at an
102 diminished intrinsic axon growth capacity of mature neurons and the hostile extrinsic environment com
103   Understanding the impact that HSV-1 has on mature neurons and the proteins most strongly associated
104 ntracellular chloride concentration found in mature neurons and thereby establishes the driving force
105 of neuronal precursors to differentiate into mature neurons and to excessive cell death.
106 licating efforts to study O-GlcNAcylation in mature neurons and to understand its roles in disease.
107 sed in neural progenitor cells, immature and matured neurons and glial cells.
108 lurane significantly decreased the number of maturing neurons and increased the number of astrocytes
109 ls are capable of differentiation, some into mature neurons, and could potentially be of value in the
110  the early neuronal marker, NeuN to identify mature neurons, and glial fibrillary acidic protein to i
111 tivation of genes that are only expressed in mature neurons, and is now found to protect the genome o
112 creased nestin expressing neural stem cells, mature neurons, and oligodendrocytes by 33, 75, and 30%,
113  on neuron projections, at the presynapse in mature neurons, and on the soma of immature neurons in t
114  several proteins that distinguish them from mature neurons, and the promoters for these genes have b
115 immature neurons with a slight effect on the mature neurons; and 5) delta-opioid receptor activation
116                     In some areas of the OE, mature neurons are absent, or sparse, although those sam
117 dual human neural precursor cells (NPC) into mature neurons are currently not fully understood.
118  proliferation and it is relatively short as mature neurons are generated between differentiation day
119                            Not knowing which mature neurons are made by specific INPs, however, conce
120 r events required for robust regeneration of mature neurons are not fully understood, particularly in
121                                      Because mature neurons are not readily regenerated, recovery fro
122 ntiation and development and the activity of mature neurons are significantly determined and regulate
123 nhibitory extracellular matrices form around mature neurons as perineuronal nets containing chondroit
124  short- and long-term synaptic plasticity in mature neurons as well as for the survival of cortical n
125        We further show that AICD increase in mature neurons, as reported in AD, alters synaptic NMDAR
126 ed iNSCs differentiate into several types of mature neurons, as well as astrocytes and oligodendrocyt
127  SynI relocation to extrasynaptic regions of mature neurons, as well as SynI dispersion from synaptic
128 ally illustrate how the apoptotic pathway in mature neurons becomes increasingly restricted by a nove
129 onal maturation status, with differentiated, mature neurons being more resistant to infection than un
130 pressed in multipotent neural precursors and mature neurons but is not detectable in glia.
131  EGR1 binding sites become hypomethylated in mature neurons but remain heavily methylated 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 g to improve growth-factor responsiveness in mature neurons by dedifferentiation, we overexpressed Li
139 tivation decreased alphavirus replication in mature neurons by regulating protein synthesis and limit
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                                  However, in mature neurons, cyclin A2 colocalized with dendritic rRN
145 cation, infects neural progenitor cells over mature neurons, decreases both populations, causes prema
146                                           In mature neurons, dendritic vesicles that entered the base
147 work, we describe a presynaptic phenotype in mature neurons derived from MAP1B knockout (MAP1B KO) mi
148                                           In mature neurons, DLK is present in the synapse and intera
149 A(A) receptor deficit induced selectively in mature neurons during adolescence lacked neurogenic and
150 id decarboxylase and tyrosine hydroxylase in mature neurons during early and late differentiation of
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                Whereas PV-evoked currents in mature neurons exhibit hallmark fast rise and decay phas
156                                              Mature neurons express a large number of distinct miRNAs
157                                              Mature neurons express MAP1B, and its deficiency does no
158 of neuronal progenitors and nascent, but not mature, neurons express INSM1.
159                                         Most mature neurons expressed only one of the ~1000 odorant r
160 cation and expression of secreted factors in mature neurons for extrinsic modulation of neurogenesis
161 MAP kinase cascade is required to switch the mature neuron from an aplastic state to a state capable
162 dult neurogenesis, the process of generating mature neurons from adult neural stem cells, proceeds co
163 dult neurogenesis, the process of generating mature neurons from neuronal progenitor cells, makes cri
164 s and immature neurons, and DeltaOMP-eGFP(+) mature neurons from normal adult mice.
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 transcriptional and functional plasticity in mature neurons has been technically challenging to addre
168 ological development of synaptic inputs onto maturing neurons has restricted our understanding of how
169                                              Mature neurons have diminished intrinsic regenerative ca
170 dex during neurogenesis and the long life of mature neurons highlight the need for efficient cellular
171                                           In mature neurons, however, presynaptic boutons are mostly
172 SAP102 is highly expressed in both young and mature neurons; however, little is known about its local
173 ignaling, which is in sharp contrast to most mature neurons hyperpolarized by GABA.
174   AAV r3.45 was more selective for NSCs than mature neurons in a human embryonic stem cell-derived cu
175 urogenesis modifies synaptic transmission to mature neurons in a manner consistent with a redistribut
176 ice) that expressed high levels of EC-SOD in mature neurons in an otherwise EC-SOD-deficient environm
177  we provide evidence that P7C3 also protects mature neurons in brain regions outside of the hippocamp
178 sis confirmed no significant increase of new mature neurons in hippocampi of TgCRND8 compared with WT
179  We also unmasked slow spillover currents in mature neurons in the absence of fast GPSCs.
180 in slices paradoxically generates spiking of mature neurons in the absence of immature neuron spiking
181  the poor intrinsic regenerative capacity in mature neurons in the adult mammalian central nervous sy
182                                              Mature neurons in the adult peripheral nervous system ca
183 eural stem cells (NSCs), astrocytes, or even mature neurons in the brains of mice can give rise to ma
184 ls (NPCs), fewer immature neurons, and fewer mature neurons in the dentate gyrus of the hippocampus o
185 hem a functional role that is different from mature neurons in the DG circuit, a distinction that pot
186 st to neurons in the central nervous system, mature neurons in the mammalian peripheral nervous syste
187 ent study, we instead focus on plasticity in mature neurons in the neocortex of adult animals.
188    After 4 weeks, the GFAP lineage generated mature neurons in the olfactory bulb (OB), DG, and, stri
189 ental continuum that results in depletion of mature neurons in the olfactory bulb.
190 proliferation, total cell numbers, number of mature neurons in the olfactory epithelium, and reactive
191 iation of multipotent neural precursors into mature neurons in vitro and that PrP(c) levels positivel
192       However, generation of physiologically mature neurons in vitro remains problematic.
193 ion offers a fast and simple method to study mature neurons in vitro, but its utility for investigati
194 in the progression of neuronal precursors to mature neurons in vivo.
195  study the effects of cell cycle re-entry on mature neurons in vivo.
196  proliferating cells and the number of newly maturing neurons in the hippocampus.
197 related activity patterns among ensembles of maturing neurons in the lateral geniculate nucleus (LGN)
198 At present, the break repair capabilities of mature neurons, in general, and rod cells, in particular
199 annels, the opposite direction compared with mature neurons, in which GABA(A) receptor activation is
200 loy the postsynaptic mechanism, whereas more mature neurons increase their strength through the presy
201                   Dendritic spine density of mature neurons increased and synaptic plasticity improve
202 verexpression of human AKAP79 in immature or mature neurons increased the number of dendritic filopod
203        An alternative hypothesis posits that maturing neurons "indirectly" contribute to memory encod
204 ique properties and structural plasticity of mature neurons induced by new-neuron integration.
205 l neurons is required for the integration of maturing neurons into the coordinated CPG network.
206       The mechanisms by which injury unlocks mature neurons' intrinsic axonal growth competence are n
207 in, not only during development, but also in mature neurons involved in long-term memory.
208 s define how the stable MT cytoskeleton of a mature neuron is converted into the dynamically growing
209 diminished intrinsic regenerative ability of mature neurons is a major contributor to regeneration fa
210                        Instead, NF-kappaB in mature neurons is activated by stimuli that induce deman
211         The mechanism by which the number of mature neurons is determined in the central nervous syst
212                        Chloride extrusion in mature neurons is largely mediated by the neuron-specifi
213 ession from neural precursor cells (NPCs) to mature neurons is tightly controlled by coordinate cell-
214 id in human, however the protocol to achieve mature neurons is time consuming.
215 and neurogenesis; however, their function in mature neurons is unknown.
216                        A critical feature of mature neurons is well-regulated endocytosis, which is v
217                                           In mature neurons, it is localized to dendritic spines, but
218 mature neurons that gradually developed into mature neurons, leading to a late increase in the volume
219                  How transient activation of mature neurons leads to long-lasting modulation of adult
220 riple-label immunofluorescence for BrdU, the mature neuron marker neuronal nuclear antigen, and the a
221  new Cr(+) or GABA(+) cells colabeled with a mature neuron marker, NeuN or chondroitin sulfate antibo
222  an Amplex Red cholesterol assay showed that mature neuron membrane cholesterol levels were significa
223                               Both young and mature neurons migrate into compartments containing astr
224                                              Mature neurons (MNs), neural progenitor cells (NPCs) and
225 nd low in newly generated neurons (NGNs) and mature neurons (MNs).
226  activation (Iba-1) increased while index of mature neurons (NeuN) significantly decreased in all bra
227 this induction is prolonged, whereas in more mature neurons, NMDA receptor stimulation induces a prot
228              In turn, overexpressing PRG5 in mature neurons not only increased Homer-positive spine n
229 or neurons, but that it is also a feature of mature neurons of both the main and accessory olfactory
230  robust, and reproducible method to generate mature neurons of many different subtypes from multiple
231 ations in the organization of newly born and mature neurons of the dentate gyrus.
232 rences in gene expression as compared to the mature neurons of the normal epithelium.
233 nd medial amygdala differentiate into either mature neurons or astrocytes.
234 lations of neuroglial stem/progenitor cells, mature neurons or epithelial-mesenchymal cells.
235 ponses of immature LGN neurons compared with mature neurons, our results show that correlated activit
236  potential for the aged stem cell to yield a mature neuron persisted at the same rate as that observe
237  in contrast to astrocytes or young neurons, maturing neurons possess negligible Nrf2-dependent antio
238                    Corresponding analysis of mature neurons predicted minimal change in neuronal exci
239 ganizer protein Satb1 is highly expressed in mature neurons, primarily in the cerebral cortex, dentat
240              Long-term potentiation (LTP) of mature neurons produces synapse enlargement balanced by
241                                           In mature neurons, Ptch and Smo are concentrated in dendrit
242                                           In mature neurons, PVs evoke GABA(A) postsynaptic currents
243 thermore, decreasing membrane cholesterol in mature neurons reduced their susceptibility to Abeta-dep
244 tially infected neural progenitor cells over mature neurons, reduced both cell populations, and cause
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                    Ablation of Tet3 in adult mature neurons resulted in increased anxiety-like behavi
254         Furthermore, knockdown of ZNF804A in mature neurons resulted in the loss of dendritic spine d
255                        Knockdown of Cap-G in mature neurons results in similar phenotypes but to a le
256                   However, after DNA damage, mature neurons resynthesize Apaf-1 through the cell cycl
257                    Morphological analysis of mature neurons revealed significantly altered neurite le
258 nduced pluripotent stem cell-derived bipolar mature neurons rotatin localizes at the centrosome in th
259                                          Why mature neurons should be particularly sensitive to such
260 ort membrane organelles is not diminished in mature neurons, suggesting that microtubule sliding is r
261  concert with reduced synaptic inhibition of mature neurons, suggesting that the local circuitry coor
262                               Differentiated mature neurons survive and control viral replication bet
263 contain disparate and fluctuating numbers of mature neurons, tactics employed by neuronal networks to
264                                           In mature neurons, TBB reduces the axodendritic polarity of
265   An interesting secondary depolarization in mature neurons that followed an initial hyperpolarizatio
266                                              Mature neurons that have experienced the overexpression
267 esults identify a unique strategy evolved by maturing neurons that uses a single microRNA to inhibit
268  express EpoR at higher levels compared with mature neurons; that Epo stimulates proliferation of emb
269                                           In mature neurons the PHR proteins also regulate axon degen
270                                           In mature neurons, the number of synapses is determined by
271 endritogenesis-associated gene expression in maturing neurons through delayed binding of NFI proteins
272 results demonstrate that CAR is expressed by mature neurons throughout the brain.
273       In addition, selective KO of Cdk5 from mature neurons throughout the hippocampus reduced the nu
274 nance of transmembrane chloride potential in mature neurons; thus KCC2 activity is critical for hyper
275 ion of NR2B-containing NMDARs at synapses of mature neurons; triple EphB knock-out mice lacking EphB1
276                                              Mature neurons typically fail to regenerate after injury
277 and mature neurons under normoxia and in the mature neurons under hypoxic condition.
278 ases (Cdks) are inappropriately activated in mature neurons under ischemic stress conditions.
279  GlyRalpha1 density in both the immature and mature neurons under normoxia and in the mature neurons
280 ed, recovery from encephalitis suggests that mature neurons utilize unique antiviral mechanisms to bl
281 f neuronal progenitor cells and a deficit in mature neurons versus wild-type animals.
282 h unoperated controls (n = 7), the number of mature neurons was about 70% higher in the paralaminar n
283           Localization of gamma-tubulin-1 in mature neurons was confirmed by immunohistochemistry and
284                  The molecular repertoire of mature neurons was sculpted by SOC-related up- and down-
285 ese mechanistic elements are widely found in mature neurons, we expect them to apply broadly to elect
286 es of immature interneurons to those of more mature neurons, we identified genes important for human
287                  As Fmrp is also enriched in mature neurons, we investigated the function of Fmrp exp
288                    Our results revealed that mature neurons were more susceptible to Abeta-induced ca
289                                      Because mature neurons were not evident at 6 wk, we examined tis
290 points, immature neuroblasts, and eventually mature neurons, were infected as determined by expressio
291 o the previously described role of CASPR2 in mature neurons, where CASPR2 organizes nodal microdomain
292 izes strongly to the axon initial segment in mature neurons, where it plays a role in assembling and
293 naptic currents (EPSCs) and spine density in mature neurons, whereas genetic ablation of neurogenesis
294  stimulates axon formation and elongation of mature neurons whether in presence or absence of inhibit
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 of how CHD proteins regulate the function of mature neurons will help better understand neurodevelopm
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

 
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