ライフサイエンスコーパス: cortical

1 ated by the organization and dynamics of the cortical actin cytoskeleton.

2 esults revealed a spatio-temporal pattern of cortical activation (i.e. travelling waves) similar to t

3 ch these statistics, a process that required cortical activity and the hypothalamic oxytocin system.

4 ers of this FOLH1 variant had less efficient cortical activity during working memory.

5 accuracy of 94.66%, and we investigated the cortical activity in response to sensory stimuli in thes

6 Decoding the world from cortical activity is strongly affected by the geometry t

7 Exaggerated prefrontal cortical activity likely underpins the inflexible thinki

8 Lastly, patterns of cortical activity that discriminated between tones becam

9 Western tonal context while recording their cortical activity using magnetoencephalography.

10 rior cingulate (PCC) and right retrosplenial cortical activity were reduced in children with NVLD rel

11 We then measured cortical activity when participants were attempting to g

12 We found that the strength of somatosensory cortical activity within the 112-252 ms time window was

13 the fourth ventricle induced NREM sleep-like cortical activity, whereas mice deficient for neurotensi

14 fness, spastic quadriparesis and progressive cortical and cerebellar atrophy in an effort to determin

15 ost pronounced in regions with major cortico-cortical and cortico-thalamic fibers: the corona radiata

16 asmic TDP-43, widespread ubiquitination, and cortical and hippocampal atrophy.

17 They add the SC to a growing number of cortical and subcortical brain areas that form distribut

18 ar regression analyses were performed for 12 cortical and subcortical gray matter regions to assess t

19 ony may facilitate such interactions between cortical and subcortical neural populations.

20 o staging of amyloid-beta deposition in both cortical and subcortical regions as a promising approach

21 d sustained recovered mGluR5 availability in cortical and subcortical regions compared with the basel

22 latory activities in a widespread network of cortical and subcortical regions.

23 exhibit altered brain networks in widespread cortical and subcortical regions.

24 growing evidence that the lack of a specific cortical architecture does not hinder advanced cognitive

25 comparison suggested that 2 to 4 times less cortical area is devoted to a penile-nerve-fiber than to

26 evoked by disparity-varying stimuli in human cortical area V3A.

27 ions of BMTK to large-scale simulations of a cortical area.

28 rk analysis of multi-omics profiling of four cortical areas across 364 donors with varying cognitive

29 es, with higher cortical thickness and lower cortical areas and volumes.

30 e intermixed and interrelated in human motor cortical areas at single-neuron resolution.

31 shes the matrix of topographically organized cortical areas available for later computational special

32 Cortical areas comprise multiple types of inhibitory int

33 x are well studied, what generates secondary cortical areas is virtually unknown.

34 Simulated patterns of involvement across cortical areas show significant overlap with the pattern

35 al transport of rabies virus to identify the cortical areas that most directly influence parasympathe

36 these circuits, we first mapped mouse visual cortical areas using intrinsic signal optical imaging an

37 w communication, particularly between visual cortical areas, is instantiated and modulated, highlight

38 l input drives the differentiation of visual cortical areas, we used two-photon calcium imaging to ch

39 nly upper layer SST+ interneurons in various cortical areas, were recently claimed to include both Ma

40 nals, originating from functionally distinct cortical areas, within crus I, paraflocculus, and vermal

41 m of sensory inputs through the hierarchy of cortical areas.

42 Therefore, cortical astrocytes respond to sensory inputs and regula

43 ephalic dogs, tissue segmentation maps and a cortical atlas generated from Jerzy Kreiner's myeloarchi

44 This comprehensive cortical atlas provides a reference standard for canine

45 estic Alzheimer's disease, 17 with posterior cortical atrophy and 22 with logopenic progressive aphas

46 ng in healthy subjects, we found progressive cortical atrophy on vertex-wise analysis in TLE before s

47 n the occipitotemporal regions for posterior cortical atrophy, left temporal lobe for logopenic progr

48 fine-grained and nuanced characterization of cortical auditory processing in the 2 hemispheres, shedd

49 n myeloid progenitors accelerates healing of cortical bone defects.

50 ation and that it is associated with thinner cortical bone in adult male mice.

51 y (SR-XRF), gadolinium was detected in human cortical bone tissue.

52 ulates synaptic function in a model of human cortical brain development.

53 ssociations in grey matter volume than other cortical brain networks.

54 ophrenia which involve aberrant increases in cortical broadband gamma activity.

55 forming a pair of recurrent cortico-thalamo-cortical (C-T-C) loops.

56 lear because experimental spatial control of cortical cell arrangement is technically challenging.

57 nchyma content, larger cortical cells, fewer cortical cell files), restrict uptake of water to conser

58 d stele-expressed SHR protein accumulates in cortical cells of M. truncatula but not Arabidopsis thal

59 nt bidirectional nutrient exchange, the root cortical cells undergo substantial transcriptional repro

60 rger proportion of stele, and smaller distal cortical cells).

61 uction (increased aerenchyma content, larger cortical cells, fewer cortical cell files), restrict upt

62 of visual selective attention involve focal cortical changes in alpha power not only for simple spat

63 d structure and activity in the same frontal cortical circuit.

64 ole in the maturation and synchronization of cortical circuitry and alterations in these inhibitory n

65 al rules underlying functional properties of cortical circuits are poorly understood.

66 So how do cortical circuits implement nonlinear representations an

67 We propose that the complexity of cortical circuits is generated by phylogenetically old i

68 developed a reduced spiking model of sensory cortical circuits that incorporated the signature short-

69 ly compromised the in vivo ability of visual cortical circuits to recover from perturbations to senso

70 To understand the function of cortical circuits, it is necessary to catalog their cell

71 ercalated and principal cell function in the cortical collecting duct (CCD).

72 sters in V3A, located within stereoselective cortical columns, responded more selectively than far-pr

73 low oscillations and increase (p < 0.001) in cortical complexity, which was similar to that observed

74 e determining which layers are involved in a cortical computation can inform us on the sources and ta

75 Cortical computations are critically reliant on their lo

76 s provide evidence of a common mechanism for cortical computations used for global integration of sti

77 y of cell types and their functional role in cortical computations.

78 Chronic pain enhances this cortico-cortical connection, as manifested by an increased numbe

79 Cortical contractility is further found to limit the cel

80 ysfunction within cortical-striatal-thalamic-cortical (CSTC) brain circuits implicated in the selecti

81 ar biology to confocal microscopy in primary cortical cultures, and from acute hippocampal and cortic

82 s, and promote organelle accumulation at the cortical cytoskeleton in normal mammary epithelial cells

83 illimeter fMRI is measuring responses across cortical depth, i.e. laminar imaging.

84 may potentially affect BOLD linearity across cortical depth.

85 rough preterm birth can significantly impact cortical development and have long-lasting adverse effec

86 gnal transduction networks critical for both cortical development and synaptic homeostasis.

87 Malformations of cortical development are a group of rare disorders commo

88 itial cell positions impact subsequent human cortical development is unclear because experimental spa

89 the JNK pathway as an important regulator of cortical development.

90 phase-coupled with DWs, and hippocampal SWR-cortical DW coupling was strengthened in post-task sleep

91 Our results suggest that the basic motifs of cortical dynamics emerge as a consequence of the efficie

92 oscillate in time as a new model to describe cortical dynamics.

93 tor of seizure freedom following surgery for cortical dysplasia.

94 d receipt, youths with DBDs showed increased cortical (e.g., OFC) and subcortical (e.g., NAcc) region

95 perfusion (gCBF), cognitive performance and cortical electroencephalography (EEG).

96 leukodystrophy-like features, and extensive cortical encephalitis evolving to atrophy.

97 multaneous elimination of YAP suppresses the cortical enlargement and folding that is induced by the

98 ticity prevents STN hyperactivity and limits cortical entrainment.

99 on mutants for defects in the degradation of cortical ER following treatment with rapamycin, a drug t

100 effects of somatosensory afferent inputs on cortical excitability and neural plasticity often used t

101 t signatures from discrete subpopulations of cortical excitatory and inhibitory neurons are significa

102 ision to the original TBM model for cerebral cortical expansion and folding.

103 By transforming normative bulk-tissue cortical expression data into cell-type expression maps,

104 Regulatory elements drive the cortical expression of SCR, and stele-expressed SHR prot

105 Furthermore, the degree of local cortical folding relates systematically with the strengt

106 as well as revise the compensation theory of cortical folding.

107 may be a causal factor in the development of cortical folding.

108 Cortical-folding complexity quantified using local gyrif

109 proposed a computational model of cerebellar cortical function based on the pioneering circuit models

110 Recent theories of cortical function construe the brain as performing hiera

111 lications for understanding the structure of cortical functional architecture.

112 re thought to act as local cues that pattern cortical Galphai, LGN, and nuclear mitotic apparatus pro

113 l surface area, cortical thickness and total cortical gray matter volumes.

114 wledge modulates processing higher up in the cortical hierarchy remains poorly understood.

115 ) power/connectivity that fed forward up the cortical hierarchy via superficial-layer cortex.

116 speech processing at different levels of the cortical hierarchy.

117 ed to analyze the presence and usefulness of cortical hypointensity on T2-weighted gradient-echo sequ

118 Long Evans male rats received a controlled cortical impact (CCI) over the caudal forelimb area (CFA

119 to sham surgery or moderate-level controlled cortical impact and infected intranasally with S. pneumo

120 nflammatory loop at 1-month after controlled cortical impact in mice by pharmacological removal of ch

121 le C57BL/6J mice at 1 month after controlled cortical impact to remove chronically activated microgli

122 f 159 patients with widely distributed focal cortical impairments, we derive lesion-deficit maps of a

123 -standing incessant ovulation hypothesis and cortical inclusion cyst involvement in sporadic ovarian

124 eir synaptic release is subject to local and cortical influence and neuromodulation.

125 ese regions as potential hubs for multimodal cortical influence.

126 Cortical inhibitory interneurons (cINs) are born in the

127 nd cortical regions, and connections between cortical inhibitory interneurons.

128 ted that high-frequency stimulation (HFS) of cortical inputs induced long-term depression (LTD) media

129 integrates a wide variety of subcortical and cortical inputs, but its synaptic organization in humans

130 ns to gate relevant and suppress distracting cortical inputs.

131 tor evoked potentials conditioned by cortico-cortical interactions between premotor ventral (PMv)-mot

132 egulation of SFs promotes BB connections and cortical interactions to organize ciliary arrays.

133 sporter three and cholecystokinin expressing cortical interneurons (CCK(+)VGluT3(+)INTs) has prompted

134 (cDKO) decreases the survival of MGE-derived cortical interneurons (CINs) and changes their physiolog

135 hological changes and abnormal allocation of cortical interneurons in vivo These data suggest that JN

136 How a dysfunction of GABAergic cortical interneurons interacts with maturation during a

137 ngential migration and laminar deposition of cortical interneurons, and further implicates the JNK pa

138 Cortical iron has been shown to be elevated in Alzheimer

139 Thus, cortical iron might act to propel cognitive deterioratio

140 Background Tumor-like cortical irregularities at the posterior distal femur ar

141 Cortical layer 1 (L1) interneurons have been proposed as

142 enia heritability with maximal enrichment in cortical layer V excitatory neurons.

143 rate successful OGB-1 AM loading of cells in cortical layers 5-6 and subsequent three-photon imaging

144 This is crucial because the different cortical layers have distinct intra- and interregional c

145 l properties resemble those of the mammalian cortical layers II/III.

146 xpression of synaptic AMPARs across multiple cortical layers in awake mice using two-photon imaging.

147 ound beta-amyloid staining, predominantly in Cortical Layers IV and VI in 27 of the 32 cats used in t

148 theories proposing that neurons in the deep cortical layers represent perceptual hypotheses and ther

149 Neurons with fbRFs are located in cortical layers that receive strong feedback projections

150 A functions as a specific marker of the deep cortical layers until the first postnatal week.

151 ium (AId), an avian analog of mammalian deep cortical layers with involvement in motor function.

152 activate layer 4 first and sequentially all cortical layers, and MMN is elicited independent of the

153 s." Different models have suggested distinct cortical layers, and rhythms implement predictive coding

154 igate the way these signals flow through the cortical layers.

155 proteolipid protein (myelin) and scored for cortical lesion types I-IV (mixed grey matter/white matt

156 Cortical lesions and the annualized cortical thinning we

157 Cortical lesions represent a hallmark of multiple sclero

158 Histopathologically, 224 cortical lesions were detected, of which the majority we

159 cts 18% of all histopathologically validated cortical lesions.

160 In this regard, at the cortical level, oxytocin can modulate the GABAergic tran

161 ance and aberrant synaptic plasticity at the cortical level.

162 extent and duration of IEDs at the scalp and cortical levels using HD-EEG source-localization, during

163 values were calculated in the neocortex and cortical lobes, basal ganglia (BG), hippocampi, and thal

164 hanisms of transcriptional dysregulation and cortical maldevelopment are reviewed, along with potenti

165 Cortical malformations arise during embryonic developmen

166 imately twofold within the cellular range of cortical mechanical tension, rendering alpha-actinin-4 a

167 Cortical mechanisms of sensory and affective integration

168 rollable transgenic mouse line that sustains cortical MET signaling.

169 tes OD plasticity independent of a canonical cortical microcircuit.

170 U2, thus regulating the lateral stability of cortical microtubules.

171 reased interhemispheric connectivity between cortical motor networks independent of individual defici

172 nterstitial fibrosis/tubular atrophy, larger cortical nephron size (but not nephron number), and smal

173 e for the hippocampus and a Posterior Medial cortical network in signaling event boundaries.

174 PNNs restrict cortical network plasticity but the molecular mechanisms

175 Norepinephrine adjusts sensory processing in cortical networks and gates plasticity enabling adaptive

176 nctional connectivity (iFC) between distinct cortical networks and thalamic nuclei are among the most

177 sistent with a growing body of evidence that cortical networks are particularly vulnerable to mutatio

178 mory consolidation mechanisms in hippocampal-cortical networks could account for spatial memory defic

179 dulated connectivity in distinct hippocampal-cortical networks depending on the category of the conso

180 w claustrum neurons broadcast information to cortical networks remain incompletely understood.

181 tide-expressing interneurons with long-range cortical networks.

182 o this end, this work investigates how motor cortical neural activity changes when three human partic

183 ehavioral abnormalities as well as increased cortical neural activity in MIA male offspring.

184 ing delivery of Task3 mRNA to distal primary cortical neurites.

185 Here, we integrated cortical neuroimaging data from patients with neurodevel

186 A reduction of p53 also partially rescued cortical neuron loss.

187 Understanding the effects of anesthesia on cortical neuronal spiking and information transfer could

188 number of WMNsST with labeled claustral and cortical neurons and also estimated their proportion in

189 s mapping fundamentally shapes the tuning of cortical neurons and corresponding aspects of perception

190 n wild-type mice enhanced the firing rate of cortical neurons and gamma oscillations, as well as impr

191 However, the spiking behavior of cortical neurons associated with such state changes has

192 In the most immature ferrets, cortical neurons developed selectivity to these patterns

193 Excitatory cortical neurons from both patients had prolonged action

194 neurotrophic factor (BDNF)-induced pTRKB in cortical neurons in culture.

195 required for the survival of hippocampal and cortical neurons in mice.

196 Cortical neurons process information on multiple timesca

197 Some cortical neurons receive highly selective thalamocortica

198 A subset of autism-iPSC cortical neurons were RNA-sequenced to reveal autism-spe

199 orically analyzed the encoding properties of cortical neurons without considering cell types.

200 f the AMPARGluA1 in HEK293 cells and primary cortical neurons, and decreases AMPAR-mediated currents

201 study of single-cell RNA sequencing of mouse cortical neurons.

202 m excitatory, glutamatergic synapses on host cortical neurons.

203 d in an in vitro model of cellular injury on cortical neurons.

204 dbrain tegmentum across patients, but not in cortical or basal ganglia regions.

205 on open new avenues of enquiry regarding the cortical organization of this tactile system.

206 Cortical organoids are self-organizing three-dimensional

207 then assembled these organoids with cerebral cortical organoids in three-dimensional cultures to form

208 etic excitation and inhibition of cerebellar cortical output neurons, Purkinje cells, attenuated seiz

209 Most notably, changes in cortical oxy-haemoglobin during a Japanese phonetic flue

210 Cortical parallel processing streams segregate many dive

211 contribution of local dynamics and inputs to cortical pattern generation during a prehension task in

212 ficient to translate interphase shape into a cortical pattern that can be read by the spindle, which

213 cues that are commonly implicated in dorsal (cortical) patterning(5) in the hypothalamus.

214 Cortical perfusion and CA impairment were heterogeneousl

215 lthood.SIGNIFICANCE STATEMENT The decline of cortical plasticity after closure of juvenile critical p

216 ve method for enhancing experience-dependent cortical plasticity as well as functional recovery in ad

217 atments for tinnitus may need to enhance the cortical plasticity, rather than reverse it.

218 c populations showed better performance than cortical populations at each SNR.

219 ediate complex interactions with the brain's cortical processing hierarchy.

220 ity could reflect a circuit that prioritizes cortical processing of events detected subcortically.

221 of facial attractiveness after 150-200 ms of cortical processing.

222 window is widely regarded to be crucial for cortical processing.

223 ontribute to contextual modulation of visual cortical processing.

224 bility of self-renewal or differentiation of cortical progenitor behaviors in vivo, a variable we hav

225 ical tubulin Tuba8, transiently expressed in cortical progenitors, drives differentiation of RGs into

226 ly acquired miRNA in eutherians that refines cortical projection neuron subtype development.

227 s from thalamocortical, deep cerebellar, and cortical projection neurons, validating transfer learnin

228 s of direct feedforward and feedback cortico-cortical projections.

229 A visual cortical prosthesis (VCP) has long been proposed as a st

230 postnatal development of dendritic arbors of cortical pyramidal neurons and the influence of experien

231 oherence are computed between macaque visual cortical recordings and their correlation with task perf

232 ay be influenced early in song learning by a cortical region (NIf) at the interface between auditory

233 and inhibition and was more prominent in the cortical region distal to the microgyrus.

234 mine early postnatal changes in this initial cortical region of the olfactory system.

235 Knowledge about the precise cortical regions and connections supporting this control

236 ues, but to different degrees, with multiple cortical regions and neostriatum tending to have the gre

237 Remarkably, cortical regions contributing heavily to the prediction

238 A mega-analysis investigating all cortical regions in a large sample of PTSD and control s

239 as well as neural ensembles within multiple cortical regions over two hemispheres of the awake mouse

240 y mid-level regions, while some higher-order cortical regions took more than 10 seconds to align.

241 ocular dominance, involving subcortical and cortical regions, and connections between cortical inhib

242 reveals that, across this diverse series of cortical regions, L5 commonly projects to multiple thala

243 that tau preferentially spreads to specific cortical regions, likely through functional connections,

244 ake in all disease groups, across widespread cortical regions.

245 known about cholinergic influences on motor cortical regions.

246 r modules projecting to functionally related cortical regions.

247 ptor-mediated high-frequency oscillations in cortical regions.

248 a but were also found in three other frontal cortical regions: lateral orbitofrontal cortex (orbital

249 ntial for understanding its possible role in cortical reorganization.

250 l inputs are necessary to maintain a precise cortical representation of space.

251 he patterns of subcortical connectivity with cortical resting-state networks (RSNs) in awake marmoset

252 pes track gene down-regulation in postmortem cortical samples of patients with depression.

253 thin the striatum, and hyper-excitability of cortical sensorimotor regions that might contribute to t

254 ement of the input-output recruitment curve, cortical silent period, and amplitude of the motor evoke

255 ent nucleator Arp2/3 complex is activated at cortical sites in Schizosaccharomyces pombe to assemble

256 cal cultures, and from acute hippocampal and cortical slices from male wild-type and amyloid precurso

257 In vivo opto-activation of cortical somatostatin interneurons alleviates motor symp

258 these results demonstrate that activation of cortical somatostatin interneurons may constitute a less

259 Further, we localized the cortical sources and observed early strong activation of

260 Conversely, this recruitment of deprived cortical space has been hypothesized to underlie phenoty

261 eorganization is the recruitment of deprived cortical space which likely aids processing and thus enh

262 ncogenic Ras(V12)-mediated cell rounding and cortical stiffening promote cell division under confined

263 iated with the following: dysfunction within cortical-striatal-thalamic-cortical (CSTC) brain circuit

264 , olfactory areas, hippocampal formation and cortical subplate.

265 Cortical superficial siderosis appears to be the result

266 In fact, cortical superficial siderosis is emerging as a strong i

267 relates and pathophysiological mechanisms of cortical superficial siderosis remain elusive.

268 Increased severity of cortical superficial siderosis was associated with upreg

269 Cortical surface area (SA), however, showed pervasive re

270 t GI in canids is positively correlated with cortical surface area, cortical thickness and total cort

271 linear model tests were conducted across the cortical surface to investigate whether PTSD and ELT exp

272 courses and information content of two major cortical systems-the multiple-demand (MD) and default mo

273 ally, geniculate axons innervated excitatory cortical targets in a preferential manner and with large

274 referentially colocalized with thalamic over cortical terminals in both the striosome and matrix comp

275 isphere, possibly suggesting competition for cortical territory due to the demand for representation

276 We found that cortical theta-gamma coupling was reduced in both male a

277 We examined aging trajectories of cortical thickness (CTh) and surface area in C9orf72 exp

278 t exposure, PTSD, and prior head injuries on cortical thickness (Monte Carlo corrected for multiple c

279 ing, and lower cognitive scores, with higher cortical thickness and lower cortical areas and volumes.

280 al cord and brain of the 9-Hole Peg Test and cortical thickness and spinal cord grey matter cross-sec

281 l intracranial volume and global measures of cortical thickness and surface area had the highest cano

282 ively correlated with cortical surface area, cortical thickness and total cortical gray matter volume

283 n children and adolescents, and ASD-specific cortical thickness differences in the frontal cortex in

284 d imaging (n = 333), subcortical volumes and cortical thickness in frontal-executive and corticolimbi

285 ect atrophy maps were generated by comparing cortical thickness in patients with CBS versus controls.

286 iomechanical studies predict an influence of cortical thickness on folding patterns.

287 oduced a more uniform DCS-LTD throughout the cortical thickness or at least abolished DCS-LTP.

288 Whole-brain analyses of cortical thickness were conducted both with and without

289 to shared genetic factors) in interregional cortical thickness, and biomechanical studies predict an

290 suggest that patterned genetic influences on cortical thickness, measurable at the scale of in vivo M

291 ized by local morphological features such as cortical thickness, myelin content, and gene expression

292 Compared to ageing-related cortical thinning in healthy subjects, we found progress

293 Cortical thinning was the primary determinant of the Exp

294 Cortical lesions and the annualized cortical thinning were also evaluated.

295 ation, and RNA transcription data from human cortical tissue samples of 233 subjects, and we detected

296 a common information space and idiosyncratic cortical topographies, and discuss implications for unde

297 ilarities between pattern vectors, and model cortical topography as mixtures of overlapping, individu

298 sitional information for the organization of cortical V1 projections onto the retinal map (Savier et

299 tients had corresponding hypermetabolism and cortical volume increase in the extrastriate visual cort

300 pagation is assumed to occur through cortico-cortical white matter connections.