ライフサイエンスコーパス: neocortical

1 AD had similar severity and distribution of neocortical Abeta compared to AD (F(1, 40-43) = 1.6-2.0,

2 However, neocortical Abeta pathology occurs many years before neo

3 eline robustly induces both cholinergic-like neocortical activation and desynchronization of function

4 , contrary to the unidirectional hypothesis, neocortical activation exhibited a continuum of activati

5 Rs arise 'spontaneously' in the hippocampus, neocortical activation often precedes SWRs and may thus

6 Changes in neocortical activity can precede SWR events, but whether

7 sk, with enhanced subcortical but suppressed neocortical activity during engagement.

8 Stable neocortical activity is asynchronous, critical, and low

9 fMRI to concurrently assess hippocampal and neocortical activity related to source memory and patter

10 is that in slow-wave sleep, replay of waking neocortical activity under hippocampal guidance leads to

11 pears far more sensitive to these drugs than neocortical activity.

12 ith isoflurane in rodents and then created a neocortical acute seizure focus with injection of 4-amin

13 While limbic and neocortical alpha-synuclein pathology had the strongest

14 We find that neocortical alpha/beta (8 to 20 Hz) power decreases reli

15 e 2 processes are thought to be supported by neocortical alpha/beta desynchronization and hippocampal

16 increases reliably precede and predict later neocortical alpha/beta power decreases.

17 urrent neuronal population, we find that the neocortical alternations reflect a dynamical regime in w

18 r than p-tau181 with CSF and PET measures of neocortical amyloid-beta burden and more accurately dist

19 From AAV injections into 42 neocortical and allocortical areas, we conclude that mos

20 Neocortical and entorhinal networks show tonic-clonic-li

21 liest epileptiform activity is restricted to neocortical and entorhinal networks.

22 Local neocortical and hippocampal territories show different a

23 ume was approximately 2- to 3-fold higher in neocortical and medial temporal brain regions of AD subj

24 ility for flortaucipir F 18 was found across neocortical and mesial temporal lobe structures.

25 revealed that xanomeline robustly decreased neocortical and striatal connectivity but induces focal

26 a-amyloid (Abeta), and SYN histopathology in neocortical and subcortical/limbic regions were compared

27 ns is held back, mechanisms that pattern the neocortical area map in the mouse could be conserved acr

28 establish the rostral to caudal axis of the neocortical area map.

29 e the cellular temporal changes and distinct neocortical areas across development.

30 The interactions between neocortical areas are fluid and state-dependent, but how

31 hat set up the specialized processing within neocortical areas during postnatal development.SIGNIFICA

32 ote memories, including higher engagement of neocortical areas during retrieval, contextual generaliz

33 ated during offline periods such as sleep to neocortical areas for long-term storage.

34 e contributions of hippocampal subfields and neocortical areas to pattern separation and source memor

35 ssion of transcription factors that position neocortical areas, and control hippocampal development.

36 -beta42 tended to accumulate more in several neocortical areas, including frontal cortices.

37 tion of upper and lower motor neurons and of neocortical areas, respectively.

38 comparison, alterations in tracts connecting neocortical areas, such as the uncinate fasciculus, were

39 However, few studies have included neocortical areas, which are challenging to assess with

40 uded limbic structures, thalamus and certain neocortical areas, which is consistent with prior studie

41 actions between prefrontal cortex and remote neocortical areas.

42 oid beta (Abeta) plaques in the striatum and neocortical areas.

43 d inputs from and sent outputs to widespread neocortical areas.

44 y encompassing lateral or medial associative neocortical areas.

45 cytoarchitectures that characterize distinct neocortical areas.

46 odium transients that were twice as large in neocortical as in hippocampal astrocytes, despite simila

47 Moreover, neocortical astrocytes experience NMDA-receptor-mediated

48 Neocortical astrocytes respond with much larger sodium e

49 d by local calcium signaling in processes of neocortical astrocytes, which is augmented by sodium-dri

50 ked local calcium transients in processes of neocortical astrocytes, which were dampened upon blockin

51 or the generation of local calcium influx in neocortical astrocytes.SIGNIFICANCE STATEMENT Astrocyte

52 e non-linear trajectories of hippocampal and neocortical atrophy in Alzheimer's disease and primary a

53 ring the interaction between subcortical and neocortical attentional networks would provide useful in

54 Neocortical basal radial glia (bRG) and cerebellar Bergm

55 sses of GABAergic interneurons of layer 5 in neocortical brain slices obtained from rats of both sexe

56 intracellular recordings in rat (both sexes) neocortical brain slices to assess the ionic mechanisms

57 Neocortical, but not hippocampal, astrocytes exhibited m

58 rs results in prominent sodium transients in neocortical, but not hippocampal, astrocytes in the mous

59 Neocortical cells form classes that likely take on uniqu

60 We found that neocortical cells were capable of forming the selectivit

61 Moreover, regional rates of neocortical change differed by phenotype.

62 e patterns of initial atrophy and subsequent neocortical change that correlated with cognitive declin

63 index increased during the arousal itself in neocortical channels, and was strongly correlated with t

64 ween hippocampal chandelier cells (ChCs) and neocortical ChCs.

65 Neocortical choline acetyltransferase (ChAT)-expressing

66 HNN's core is a neocortical circuit model that accounts for biophysical

67 A basic-yet nontrivial-function which neocortical circuitry must satisfy is the ability to mai

68 napse-type and layer specific changes in the neocortical circuitry of FMR1 knockout mice.

69 Neocortical circuits are sensitive to experience, showin

70 Neocortical circuits consist of stereotypical motifs tha

71 spontaneous ictal events in hippocampal and neocortical circuits in experimental models of chronic t

72 Neocortical circuits use a family of homeostatic plastic

73 rse of postnatal maturation to that in other neocortical circuits, but also implies that consideratio

74 contextual information is a core feature of neocortical circuits.

75 f intellectual disability, is known to alter neocortical circuits.

76 ce-dependent development of specific sensory neocortical circuits.

77 act to determine the development of specific neocortical circuits.

78 ergic inhibitory interneurons throughout the neocortical column during active sensation.

79 Precuneus cTBS altered MTL-neocortical communication by modulating theta and gamma

80 consolidation requires coherent hippocampal-neocortical communication mediated by PV(+) cells.

81 of declarative memories requires hippocampal-neocortical communication.

82 Sensory perception depends on neocortical computations that contextually adjust sensor

83 e human claustrum, a major hub of widespread neocortical connections, is a thin, bilateral sheet of g

84 irments in neonatal vocalizations as well as neocortical cytoarchitectonic alterations via neuronal p

85 Alteration of neocortical cytoarchitecture, such as disruption of the

86 nd reliable upstream event of entorhinal and neocortical degeneration, calling into question a prevai

87 port that calcium activity in populations of neocortical dendrites is increased and synchronised duri

88 pecific expression trajectories across human neocortical development and aging; classes I, II, and IV

89 of the psychiatric risk gene, NRG3, in human neocortical development and expand on previous findings

90 e critical and diverse functions of WDR62 in neocortical development and provide insight into the mec

91 specific roles of Tcf4 molecular pathway in neocortical development and their relevance in the patho

92 adial glia progenitors is critical to proper neocortical development but the mechanisms regulating th

93 is model retains essential features of human neocortical development by encompassing a single self-or

94 lution across the first two decades of human neocortical development in NeuN+ neurons using whole-gen

95 strate that CLASP2 has distinct roles during neocortical development regulating neuron production and

96 f neural stem-progenitor cells (NPCs) during neocortical development, and thus reduced the number of

97 compare the functions of CTIP2 and SATB2 in neocortical development, between the eutherian mouse and

98 During neocortical development, neurons are produced by a diver

99 ing to brain development and, in particular, neocortical development, we generated forebrain-specific

100 ays a key role in maintenance of NPCs during neocortical development.

101 c dynein participates in multiple aspects of neocortical development.

102 al determinant of radial glial tiling during neocortical development.

103 trinsic and global functions for Lgl1 during neocortical development.

104 e show here that the IGF-1R is essential for neocortical development.

105 g pathway plays a crucial role in regulating neocortical development.

106 emories may in fact initiate the hippocampal-neocortical dialog, whereas reactivation of newer memori

107 ons, which actively dictates the hippocampal-neocortical dialogue and information transfer.

108 veal important insights into the hippocampal-neocortical dialogue, which is of key importance for mem

109 Importantly, these hippocampal-neocortical dynamics were particularly pronounced during

110 ar activating system (ARAS), contributing to neocortical dysfunction and neurocognitive impairments.

111 accomplishes this by assembling consolidated neocortical elements into spatially coherent scenes that

112 izure frequency in a male rat model of focal neocortical epilepsy characterized by discrete spontaneo

113 nt epilepsy and are the most common cause of neocortical epilepsy in children.

114 tic effectiveness in a rodent model of focal neocortical epilepsy.

115 formation shares conserved features of human neocortical expansion.

116 issencephalic rodents but critical for human neocortical expansion.

117 ng that Sox9 may have contributed to promote neocortical expansion.

118 y decreased hippocampal firing and increased neocortical firing, in both regions firing rate distribu

119 Although high neocortical flortaucipir retention was consistently asso

120 fferences in regional or composite posterior neocortical flortaucipir standard uptake value ratio as

121 When we reduce the concentration of neocortical GABA using trans-cranial direct current stim

122 ese findings establish a predictive model of neocortical GABAergic interneuron myelination determined

123 lls form the second largest subpopulation of neocortical GABAergic neurons that contain diverse subty

124 its in males were negatively correlated with neocortical GABAergic synaptic gene expression.

125 ation of chromatin structure and function in neocortical GABAergic, glutamatergic, and monoaminergic

126 Neocortical gamma activity has long been hypothesized as

127 , analysis, and functional interpretation of neocortical gamma-range activity.

128 By adulthood, neocortical glial cell density and gene expression were

129 sharpwave ripples (HC-SWRs), correlated with neocortical graphoelements (NC-GEs).

130 ad higher 11C-PBB3 binding capacities in the neocortical grey and white matter segments than healthy

131 interactions that have long-range effects on neocortical gyrification and shows that lissencephaly in

132 The extent of neocortical gyrification is an important determinant of

133 losum, a large axon tract connecting the two neocortical hemispheres that emerged exclusively in euth

134 Neocortical-hippocampal interactions support new episodi

135 nderlying active consolidation, comprising a neocortical-hippocampal-neocortical reactivation loop in

136 n amyotrophic lateral sclerosis (ALS) and to neocortical hyperexcitability, a prominent feature of bo

137 chemes were constructed, and hippocampal and neocortical (inferior temporal and middle frontal) brain

138 may thus constitute a trigger event in which neocortical information seeds associative reactivation o

139 t memories using relational information, and neocortical inhibition prevents unwanted co-activation b

140 The second mechanism involves neocortical inhibition.

141 Neocortical inhibitory neurons exhibit remarkably divers

142 tatory inputs to major archetypal classes of neocortical inhibitory neurons, fast-spiking (FS) and no

143 M), two markers of particular sub-classes of neocortical inhibitory neurons.

144 re a major trigger of spontaneous release at neocortical inhibitory synapses but not at excitatory sy

145 , we report that segmental myelination along neocortical interneuron axons is strongly predicted by t

146 y neurons and parvalbumin-positive GABAergic neocortical interneurons (PV-INs) during naturalistic se

147 Spatially clustered neocortical interneurons originating from low-titre retr

148 that control the functional organization of neocortical interneurons remain largely unknown.

149 napse formation and microcircuit assembly of neocortical interneurons.

150 shapes the RNA expression patterns of adult neocortical interneurons.

151 lesionectomy with tailoring for surrounding neocortical involvement.

152 proaches: hippocampectomy with tailoring for neocortical involvement; lesionectomy of temporal lesion

153 lest terms, this theory postulates a central neocortical island (6 layers) separated by a surrounding

154 erlying the processing of top-down inputs in neocortical L1.

155 Neocortical layer 1 (L1) is the main target of cortical

156 unprecedented detail.SIGNIFICANCE STATEMENT Neocortical layer 1 (L1) is the main target of corticoco

157 leads to increased neuronal excitability of neocortical layer 2/3 (L2/3) pyramidal neurons.

158 tic properties of dendritic Ca(2+) spikes in neocortical layer 5 pyramidal neurons.

159 combinase in corticothalamic (CT) neurons in neocortical layer 6.

160 d neuron production but essential for timing neocortical layer formation and specifying laminar fates

161 ost powerful inhibitory input of PV cells in neocortical layer V.

162 cessfully record neuronal activity in deeper neocortical layers and parts of the hippocampus in roden

163 Autapses in neocortical layers have not been systematically investig

164 ical characterization is presented in AD and neocortical LBD samples using chromogenic and fluorescen

165 The moderate decrease in neocortical LBD suggests the effect of coexisting AD pat

166 tween the mean grey values of CNT vs. AD and neocortical LBD vs. AD.

167 in every cortical layer compared to CNT and neocortical LBD.

168 Diffuse (neocortical) LBD was associated with shorter disease dur

169 , SE = 0.002, p = 0.002) and in persons with neocortical Lewy bodies (estimate for interaction = -0.1

170 sed beta-amyloid burden, tau tangle density, neocortical Lewy bodies, hippocampal sclerosis, chronic

171 Alzheimer's disease (AD) and neocortical Lewy body disease (LBD) are the most common

172 ersons with more tau tangle density and with neocortical Lewy body pathologies.

173 ly calculated in 12 brain regions, including neocortical, limbic and subcortical areas from Alzheimer

174 ccumulation of amyloid-beta (Abeta) promotes neocortical MAPT (tau) aggregation in familial and idiop

175 sh expectations for future experience within neocortical-medial temporal lobe circuits.

176 wever, the engrams and circuits that support neocortical memory consolidation have thus far been unkn

177 s-cranial direct current stimulation (tDCS), neocortical memory interference increases in proportion

178 diating the stabilization of hippocampal and neocortical memory traces.

179 Our data help understand how wS1 neocortical microcircuits might process and integrate se

180 While proliferation of resident neocortical microglia under homeostatic conditions was l

181 ly, the way in which regional differences in neocortical migration are controlled is completely unkno

182 Here, we tested a key potential node in neocortical model formation in this process, layer (L) 6

183 frontal cortex (mPFC; a critical node of the neocortical network supporting long-term memory storage)

184 rticographic recordings across a 10-cm-sized neocortical network.

185 presentations of neural codes of hippocampal-neocortical networks during sleep would reveal important

186 formation and are gradually consolidated in neocortical networks for permanent storage.

187 us and only gradually become instantiated in neocortical networks over a period of weeks to years.

188 unction mediated by FS and non-FS neurons in neocortical networks.

189 unction mediated by FS and non-FS neurons in neocortical networks.SIGNIFICANCE STATEMENT Dynamic bala

190 Moreover, we show that a hippocampal-neocortical neurocomputational model based on this assum

191 er, chimpanzee tissue is inaccessible during neocortical neurogenesis when differences in brain size

192 pressed and derepressed mRNA isoforms during neocortical neurogenesis whose orthologs include risk ge

193 d gene expression data representing distinct neocortical neuron classes in Mus musculus and interneur

194 g, localize to >20 excitatory and inhibitory neocortical neuron types defined by physiology, morpholo

195 Single neocortical neurons are driven by populations of excitat

196 clamp recordings from the dendrites of human neocortical neurons have recently been reported by Beaul

197 Single-cell transcriptomics of neocortical neurons have revealed more than 100 clusters

198 NQ2 channels in regulating the properties of neocortical neurons is largely unexplored.

199 However, the role of Foxp2 in neocortical neurons is poorly understood.

200 nstructions of the twelve main categories of neocortical neurons to derive the dependence of activati

201 ed excitatory postsynaptic responses in most neocortical neurons, but elicited action potentials prim

202 a single-cell RNA-seq study of 22,439 mouse neocortical neurons.

203 1 but not in CA3 hippocampal or layer II/III neocortical neurons.

204 the variable cerebellar, basal ganglia, and neocortical neuropathology with the variability of motor

205 Pafah1b1-deficient neocortical NPCs and MEFs similarly exhibited cleavage p

206 Here, we report the sliced neocortical organoid (SNO) system, which bypasses the di

207 human pluripotent stem cell (hPSC)-based 3D neocortical organoid model.

208 Using hPSC 3D neocortical organoids, we demonstrate that the effects o

209 erience with sequencing relationships affect neocortical oscillations and neuronal responses is poorl

210 t particles in the pial arterial wall and in neocortical parenchyma of young, drug-resistant epilepsy

211 ely perceived event boundaries and shifts in neocortical patterns underlying belief states.

212 iple biochemical pathways collectively shape neocortical plasticity is missing.

213 Using RNA-seq analysis of mouse neocortical polysomes, here we report translationally re

214 ng NREM sleep in the rodent, hippocampal and neocortical populations are excitable: each in a stable

215 The neocortical postsynaptic proteome data resource can be u

216 mulus-driven L6 neurons are required to form neocortical predictions, and to realize their behavioral

217 The contribution of this pathway to neocortical preparatory signals remains poorly understoo

218 e peak period of FGF8 signaling in the mouse neocortical primordium (NP), the NP was the same size in

219 ty closely followed the patterns observed in neocortical principal cells rather than the hippocampal

220 on of reactive oxygen species, inhibition of neocortical progenitor cell proliferation, induction of

221 fy a diversity in the temporal plasticity of neocortical progenitors, revealing that some subtypes of

222 derived fibroblasts, which, similar to mouse neocortical progenitors, transiently arrest at prometaph

223 Their functions in the migration of neocortical projection neurons, however, are unclear.

224 ges, sites of ZIKV replication including the neocortical proliferative zone and radial columns, as we

225 s a critical CAM required for innervation of neocortical PyN AISs by ChCs.

226 c activation was used to examine the role of neocortical pyramidal cells in generating spasms.

227 Chemogenetic activation of neocortical pyramidal cells supported these observations

228 channels contributes to persistent firing in neocortical pyramidal cells.

229 sms can be induced in tandem in cultured rat neocortical pyramidal neurons by chronic manipulations o

230 equences as a result of KCNQ2 dysfunction in neocortical pyramidal neurons is still unknown.

231 Neocortical pyramidal neurons regulate firing around a s

232 which may help to explain the morphology of neocortical pyramidal neurons.

233 tions in Scn8a(N1768D/+) CA1, but not CA3 or neocortical, pyramidal cells was significantly reduced c

234 g, findings were observed between TDP-43 and neocortical rates.

235 dation, comprising a neocortical-hippocampal-neocortical reactivation loop initiated by the neocortex

236 n was higher in SYN + AD than SYN-AD in each neocortical region (F(1, 54) = 5.6-6.0, p < 0.02) but wa

237 ral region of interest: t = 2.86, P = 0.005; neocortical region of interest: t = 2.90, P = 0.004), yo

238 ral region of interest: t = 3.83, P < 0.001; neocortical region of interest: t = 5.01, P < 0.001).

239 e survivors with aphasia have suggested that neocortical regions adjacent to auditory cortex are prim

240 mposition of postsynaptic proteomes in human neocortical regions and integrate it with genetic, funct

241 ake was highest in the striatum, followed by neocortical regions and white matter, and lowest in the

242 ortex is common by age 60, whereas spread to neocortical regions and worsening of cognition is associ

243 y concurrent with spread of tau pathology to neocortical regions before clinical impairment.SIGNIFICA

244 ions of interneuron precursors to restricted neocortical regions belonging to the same functional are

245 ols (p<0.05, paired t-test), particularly to neocortical regions including insular, lateral frontal,

246 ed auditory system, in limbic or association neocortical regions involved in cognitive functions.

247 T signal was estimated in temporal meta- and neocortical regions of interest.

248 Neocortical regions show signatures of expression of ind

249 (18)F-PI-2620 uptake in neocortical regions significantly correlated with the de

250 ites of layer 5 pyramidal neurons of several neocortical regions that is reversed by subsequent E2 tr

251 ia basal ganglia pathways, from mood-related neocortical regions to dopamine-containing neurons of th

252 on concentration in the deep gray matter and neocortical regions was higher in patients with Alzheime

253 (18)F-PI-2620 uptake in neocortical regions was significantly correlated with th

254 oral lobe areas, but essentially also by the neocortical regions which these areas control.

255 e-infragranular neurons recorded in multiple neocortical regions, as well as deep brain structures su

256 ine in human cognitive ageing has focused on neocortical regions, the hippocampus and dopaminergic ne

257 no increased standard uptake value ratios in neocortical regions.

258 ctive neuronal cytoplasmic inclusions in the neocortical regions.

259 ficient stereological cell counting in eight neocortical regions.

260 are inversely correlated in medial temporal neocortical regions.

261 local sharp-wave ripples, and the associated neocortical replay tends to occur during local sleep spi

262 Under homeostatic conditions, we found that neocortical resident microglia were long-lived, with a m

263 does information from seconds earlier affect neocortical responses to new input?

264 tion of recently acquired memory traces into neocortical schemas through the interleaved activation o

265 those recorded during experimental and human neocortical seizures.

266 Neocortical sensory areas are thought to act as distribu

267 Time locking between neocortical sleep slow oscillations, thalamo-cortical sp

268 Acute treatment of neocortical slices with E2 also rescued the OVX-associat

269 ngs also revealed a ramp-up in the number of neocortical slow oscillations preceding spasms, which wa

270 al recordings during 4-aminopyridine-induced neocortical spikes and seizures.

271 sis confirmed elevated levels of hippocampal-neocortical spindle coupling around ripples, with direct

272 We report that the cycles of neocortical spindles provide a key temporal window that

273 ilarly, we found that Motifs were coupled to neocortical spindles, down-to-up transitions, theta burs

274 phy positive (Abeta+) subjects, flortaucipir neocortical standard uptake value ratio was significantl

275 ment by encompassing a single self-organized neocortical structure, without including an animal-deriv

276 ing the patterns of c-Fos expression in more neocortical structures of rats and marmosets using a mor

277 We measured neocortical sub- and suprathreshold dendritic membrane p

278 PBB3-positive tau inclusions at the depth of neocortical sulci, confirming 11C-PBB3 binding to tau le

279 re, we report that the claustrum coordinates neocortical SW generation.

280 patients with AD copathology harbor greater neocortical SYN pathology.

281 luorescence imaging and electrophysiology in neocortical synapses, we show that Syt1(F349A) is more e

282 mic axons are guided internally toward their neocortical target by corridor (Co) neurons that act as

283 rior temporal cortex (ITC), an early site of neocortical tau accumulation associated with AD.

284 explanation for the anatomic specificity of neocortical tau deposition in the aging brain and reveal

285 cal Abeta pathology occurs many years before neocortical tau pathology in AD.

286 e metabolism decreased when both amyloid and neocortical tau were high and predicted subsequent memor

287 Neocortical tauopathy was positively associated with met

288 Like SWRs, SSRs often co-occur with neocortical theta bursts (TBs), downstates (DSs), sleep

289 Retrieval was associated with MTL-posterior neocortical theta phase coupling and theta-gamma phase-a

290 A pattern of pervasively reduced neocortical thickness appears to be common across all fo

291 d patterns of reduced global and parcel-wise neocortical thickness nearly identical to those associat

292 ed global and widely distributed parcel-wise neocortical thickness.

293 t cells (pvBCs) in layer 2/3 (L2/3) in human neocortical tissue resected in deep-brain surgery, and i

294 reviously established computational model of neocortical tissue, and validate it as an adequate model

295 al spikes during sleep interrupt hippocampal-neocortical transfer of information.

296 ell partnerships may represent a fundamental neocortical unit of computation at the population level.

297 The identification of neocortical up states as a mechanism capable of initiati

298 and fusiform regions, as well as a posterior neocortical VOI composed of average values from parietal

299 rence region was 2.22% for a large posterior neocortical VOI, 1.84% for MUBADA, 1.46% for frontal, 1.

300 ) was calculated for a statistically defined neocortical volume of interest.