ライフサイエンスコーパス: callosal

1 Callosal abnormalities were independent of psychosocial

2 ings of deficits in bimanual coordination in callosal absence, but using significantly improved measu

3 s difference is mechanistically explained by callosal activation of fast-spiking parvalbumin-expressi

4 rozygous Nfib-deficient animals also exhibit callosal agenesis and delayed lung maturation, indicatin

5 nique defects in lung maturation and exhibit callosal agenesis and forebrain defects that are similar

6 (genetic and environmental) determining both callosal agenesis and its autistic features, and what ar

7 ised structural abnormalities, in particular callosal agenesis and pontine hypoplasia, delayed myelin

8 stinguish autistic behaviour associated with callosal agenesis from autism more generally.

9 l and cognitive impairments in subjects with callosal agenesis may overlap with the profile of autism

10 provide potential avenues for therapies for callosal agenesis or related neurodevelopmental disorder

11 directly compared a group of 26 adults with callosal agenesis to a group of 28 adults with a diagnos

12 enetic features of syndromes associated with callosal agenesis, and provides a genetic and developmen

13 erited multisystem disorder characterized by callosal agenesis, cataracts, cardiomyopathy, combined i

14 In addition to the five principal features (callosal agenesis, cataracts, hypopigmentation, cardiomy

15 igence quotient and autism symptomatology in callosal agenesis, nor evidence that the presence of any

16 odevelopmental disorders are associated with callosal agenesis.

17 lity, neocortical abnormalities, and partial callosal agenesis.

18 lectual disability and frequently displaying callosal agenesis.

19 ns and single gene mutations associated with callosal agenesis.

20 deposts and Slit2 upregulation, resulting in callosal agenesis.

21 enic mice, we first assessed hippocampal and callosal anatomy in PSAPP (PS1xAPP) mice, another transg

22 frontal cortex infiltrated juxtaposed corpus callosal and cortical tissue.

23 ound to repel cortical axons into developing callosal and corticospinal pathways.

24 tor cortex of rodents occurs largely through callosal and frontal cortical association projections di

25 to investigate the anatomical development of callosal and frontal premotor projection neurons (CPN an

26 nces between these neurons with simultaneous callosal and frontal projections during development.

27 al projection neurons maintains simultaneous callosal and frontal projections in adult mice, suggesti

28 the percentage of neurons with simultaneous callosal and frontal projections, and an isolated popula

29 Thus, Satb2 promotes the development of callosal and subcerebral neurons in a cell context-depen

30 pread abnormal diffusivity properties in the callosal and temporal lobe WM regions in individuals wit

31 ical disability in MS, and that low anterior callosal and thalamic FA have specific importance to cog

32 variety of pathways, including corticofugal, callosal, and thalamocortical tracts.

33 To assess the diagnostic performance of the callosal angle (CA) and Evans index (EI) measures and to

34 Total and parcellated midsagittal callosal areas and measures indexing vertical displaceme

35 Callosal areas did not differ between groups defined by

36 Thus, our results demonstrate that callosal as well as extracallosal anatomical connections

37 terior commissure was absent, and the corpus callosal as well as hippocampal commissural axons failed

38 Cortical pathology, callosal atrophy and axonal loss are substrates of progr

39 nal propagation and anatomical properties of callosal auditory fibers as measured with diffusion-weig

40 AC were negatively related to the volume of callosal auditory fibers.

41 Functional analysis of callosal axon conduction showed a significant improvemen

42 gen receptor beta ligand treatment to affect callosal axon demyelination and stimulate endogenous mye

43 ional functions for the sling independent of callosal axon guidance.

44 The midline glia structures important for callosal axon midline crossing appear normal in the tran

45 ost cells emitting guidance cues to instruct callosal axon navigation.

46 The meninges produce BMP7, an inhibitor of callosal axon outgrowth.

47 Callosal axon pathology progressively worsened with age

48 er positioning of migrating neurons, and the callosal axon projections important for communication be

49 understudied areas of development including callosal axon refinement.

50 decline was accompanied by brain atrophy and callosal axonal loss.

51 re, we investigate whether Slit2 also guides callosal axons after they cross the midline.

52 with the change in conductive properties of callosal axons along the anterior-posterior axis.

53 IE2(+) callosal axons also failed to cross the midline to form

54 Although callosal axons approach the midline, they fail to cross

55 mate homeostasis at a time when unmyelinated callosal axons are engaging in glutamatergic signaling w

56 ory lesion in the rat frontoparietal cortex, callosal axons become dystrophic and die back.

57 m, Slit2 expressed by the glial wedge guides callosal axons before they cross the midline, as they ap

58 pathological and functional abnormalities of callosal axons despite the presence of inflammation.

59 usly obtained by extrapolating the length of callosal axons from that of the monkey, proportionally t

60 In Neurod2/6 double-mutant mice, callosal axons lack expression of the cell adhesion mole

61 py studies revealed a marked degeneration of callosal axons long before the onset of motor symptoms.

62 ing PFP axons and contralaterally projecting callosal axons make distinct guidance decisions at the s

63 Callosal axons release glutamate by vesicular fusion, wh

64 Crossing of the midline by callosal axons relies on a proper midline environment th

65 anipulations in organotypic slices show that callosal axons require the presence and correct orientat

66 ng these results, increased vulnerability of callosal axons was documented in the brains of HD patien

67 oping chick spinal commissural axons and rat callosal axons) findings demonstrate that knockdown of K

68 d within the tract formed by these cingulate callosal axons, and appeared to fasciculate with them as

69 ry bulb and a failure of midline crossing of callosal axons.

70 neurons and turns on before outgrowth of the callosal axons.

71 ted step that occurs during remyelination of callosal axons.

72 slices to specifically analyze postcrossing callosal axons.

73 act as a guidance substratum for developing callosal axons.

74 istic extracortical features, such as corpus callosal, basal ganglia, and cerebellar abnormalities.

75 confirmed within the corticospinal tract and callosal body, and linked strongly to clinical upper mot

76 n fractional anisotropy in the left cingulum-callosal bundle.

77 fusion tract tracing (DTT) reconstruction of callosal bundles from different areas.

78 ely to determine not only the association of callosal clusters with specific sets of ODCs, but also i

79 re oligodendrocytes correlated with improved callosal conduction and refractoriness.

80 ribution of axon diameter, so as to estimate callosal conduction delays from different areas.

81 As in monkeys, in humans the shortest callosal conduction delays were those of motor, somatose

82 as a prerequisite for the computation of the callosal conduction distances and delays in humans, whic

83 It is generally thought that callosal connections (CCs) in primary visual cortices se

84 ith the nonparetic limb are mediated through callosal connections and the contralesional sensorimotor

85 uring a brief period between P4 and P6, when callosal connections are still very immature.

86 laces, we studied the topography of emerging callosal connections at and immediately after P6.

87 us, the development of the normal pattern of callosal connections depends on dorsal column input and

88 functions for EphA receptor in establishing callosal connections during brain development.

89 strated surprisingly normal distributions of callosal connections in the nondeprived right hemisphere

90 n these findings and the known physiology of callosal connections in the visual system, we developed

91 er, in rodents the overall pattern of visual callosal connections is adult-like by postnatal day 12 (

92 y site prompted us to examine whether corpus callosal connections may play a role in this transhemisp

93 The main callosal connections of M1 and the caudal portion of PMD

94 The callosal connections of motor and premotor fields in the

95 ections are somatotopically matched; and (5) Callosal connections of PV are with S2 and PV of the oth

96 this question, we examined the cortical and callosal connections of the primary somatosensory area (

97 Dc) were with homotopic sites, and the major callosal connections of the rostral portion of PMD (PMDr

98 l striate cortex, and the overall pattern of callosal connections revealed following multiple tracer

99 , LC offspring had a broader distribution of callosal connections than HC offspring and a significant

100 In BEP7 ferrets we found that the pattern of callosal connections was highly anomalous and the sizes

101 Callosal connections were mostly with the region of the

102 including direct subcortical connections and callosal connections with the contralateral hemisphere.

103 role in the development of interhemispheric callosal connections, but little is known about the role

104 ain features, including changes in raphe and callosal connections, sensory processing, and myelin she

105 ition, M1 forelimb representation had sparse callosal connections, whereas M1 trunk and face represen

106 ns, as well as the premotor areas, had dense callosal connections.

107 wo-stage pathway involving interhemispheric (callosal) connections between information processing lev

108 extract measures of structural and effective callosal connectivity between different somatosensory co

109 on to the thalamus and other ipsilateral and callosal corticocortical connections.

110 at <33 weeks gestation and who had sustained callosal damage visualized on structural MRI were compar

111 cal, periventricular subcortical lesions and callosal demyelination in relapsing-remitting experiment

112 We mapped callosal development and explored sex differences in a l

113 This defect in callosal development correlates with the expression of t

114 ouse OPC differentiation in vitro and during callosal development in vivo.

115 Even so, existing studies of callosal development tend to use parcellation schemes th

116 t1/2 double mutants display malformations in callosal development, and in corticothalamic and thalamo

117 opmental regulation of normal brain size and callosal development.

118 circuit dysfunction (n = 22), and those with callosal disconnection (n = 7).

119 circuit dysfunction (n = 22), and those with callosal disconnection (n = 7).

120 lar enlargements potentially contributing to callosal displacements were assessed as a secondary goal

121 schizophrenia probands exhibited significant callosal displacements.

122 third ventricle enlargements were related to callosal displacements.

123 In many cases of callosal dysgenesis in both human patients and mouse mod

124 unctional astroglial migration underlies the callosal dysgenesis in conditional Fgfr1 knockout mice,

125 We propose that anomalous brain circuitry of callosal dysgenesis is determined by long-distance plast

126 n this puzzle, we investigated patients with callosal dysgenesis using structural and functional neur

127 data showed that CFC mediated the effect of callosal FA on BPA.

128 allosum (DTI), individuals with low anterior callosal FA were found to exhibit greater activity in a

129 erformance for individuals with low anterior callosal FA, greater RIPFC activity during verbal encodi

130 rformance for individuals with high anterior callosal FA.

131 (RIPFC) relative to those with high anterior callosal FA.

132 are critical downstream targets of Satb2 in callosal fate specification.

133 ed the properties of the estimated occipital-callosal fiber tracts by combining them with functional

134 present and function in developing forebrain callosal fibers based on both spatial and temporal expre

135 In normal animals callosal fibers connect retinotopically corresponding, n

136 eas in rats bilaterally enucleated at birth, callosal fibers connect topographically mismatched, mirr

137 in animals bilaterally enucleated at birth, callosal fibers connect topographically mismatched, mirr

138 nt) hand correlated with higher integrity of callosal fibers connecting occipital cortices, whereas l

139 raded left posterior cingulate and posterior callosal fibers in chronic alcoholics, which is consiste

140 ecifically with the fractional anisotropy of callosal fibers interconnecting SII.

141 We segmented the callosal fibers into regions based on their likely corti

142 sivity perpendicular to the main axis of the callosal fibers that connect the temporal lobes.

143 tion primarily occurs in SII, is mediated by callosal fibers that interconnect homologous SII areas,

144 The destination of the callosal fibers was examined by applying DiI to the righ

145 l axons were examined with DiI labeling, few callosal fibers were found to traverse the midline in bo

146 ve transhemispheric propagation along corpus callosal fibers.

147 de well with the projection direction of the callosal fibers.

148 the corpus callosum: the genu, splenium and callosal fibres connecting the motor cortices.

149 cting the SMA with the striatum; and (5) SMA callosal fibres.

150 heterozygosity and Yap deletion both restore callosal formation in Nf2 mutants.

151 by abnormal interhemispheric processing and callosal functioning, but there have been no studies on

152 s each correlated with older age and smaller callosal genu (anterior) areas.

153 tter radial diffusivity predominantly in the callosal genu and body (both p < 0.003).

154 tter integrity, but it is less marked in the callosal genu and body in the offspring.

155 Callosal genu and body microstructure but not macrostruc

156 ty of major white matter tracts, such as the callosal genu and splenium, cingulum, optic radiations,

157 ignificantly associated with lower FA in the callosal genu, thalamus, right posterior cingulum, and f

158 Alternating phases of callosal growth and shrinkage may reflect a permanent ad

159 Thus, more detailed mapping of callosal growth processes is desirable to create a norma

160 ted interest in the mechanisms that regulate callosal growth.

161 Total brain, corpus callosal, hippocampal, thalamic and basal ganglia volume

162 The additional anomalies were as follows: callosal hypoplasia in 3 children, abnormalities of gyra

163 with additional cerebral anomalies including callosal hypoplasia or agenesis, abnormal basal ganglia

164 areas 17 and 18 receive selective excitatory callosal input on both ongoing and evoked activity.

165 Callosal inputs also elicit more spikes in type A neuron

166 Repeatedly stimulating callosal inputs evokes progressively smaller excitatory

167 In contrast, alcoholics who have compromised callosal integrity showed less bilateral processing adva

168 the contralateral thalamus may modulate the callosal interactions that are presumed to play a role i

169 ly, it was thought a total absence of corpus callosal interhemispheric connective tissues in the BTBR

170 onto-occipital fasciculus, internal capsule, callosal isthmus, and the corona radiata (p=0.04 for FIQ

171 brain and have referenced these maps against callosal landmarks.

172 e matter volume (P<.001), a 6.9% increase in callosal length (P =.002), a 15.3% reduction in callosal

173 Study of patients with callosal lesions can provide insight into the mediation

174 ults are consistent with the hypothesis that callosal linkages are stabilized during development by i

175 that development of retinotopically matched callosal linkages depends critically on retinal influenc

176 We found that the patterns of callosal linkages in rats enucleated at P12, P8, and P6

177 r the development of retinotopically matched callosal linkages.

178 Callosal malformations are among the most common congeni

179 the cues that determine the mirror-symmetric callosal map exert only a weak control on the topography

180 t support the idea that retinal input guides callosal map formation by primarily promoting the large-

181 bserved that the normal, nonmirror-symmetric callosal map, as well as the anomalous, mirror-symmetric

182 whether retinal input guides development of callosal maps by promoting either the corrective pruning

183 Callosal maps were revealed by placing small injections

184 Degradation of the callosal microstructure was consistently associated with

185 rface-based mesh-modeling methods to analyze callosal morphology at extremely high spatial resolution

186 etic and nongenetic contributions to altered callosal morphology in schizophrenia.

187 vironmental influences contribute to altered callosal morphology in schizophrenia.

188 ivity of the reconstructed corticospinal and callosal motor fibres compared with controls, without ch

189 Increased callosal myelination and mature oligodendrocytes correla

190 The differences in callosal myelination suggested by these results may refl

191 Finally, we hypothesize that intrinsic and callosal networks processing different orientations and

192 Satb2) is required for proper development of callosal neuron identity and represses expression of gen

193 in regulating transcriptional mechanisms of callosal neuron specification.

194 on, multiple EphA receptors are expressed in callosal neurons and ephrin-A5 stimulates neurite outgro

195 s does not influence the correlation between callosal neurons and ODCs.

196 generation of either corticofugal neurons or callosal neurons below the cortex is sufficient to recru

197 bustly to Sema3A than those from presumptive callosal neurons expressing Satb2.

198 nd ephrin-A5 stimulates neurite outgrowth of callosal neurons in vitro.

199 The misspecified callosal neurons largely fail to form the corpus callosu

200 Ski-deficient callosal neurons lose their identity and ectopically exp

201 ctive for corticospinal neurons, but affects callosal neurons within the motor cortex in motor neuron

202 ural stem cell pool and the specification of callosal neurons.

203 o significant effect on the number of visual callosal neurons.

204 d for transcriptional repression of Ctip2 in callosal neurons.

205 a significantly higher percentage of labeled callosal neurons.

206 ispensable for axonal outgrowth of layer 2/3 callosal neurons.

207 ns, and to repress subcerebral characters in callosal neurons.

208 ection in a subset of early born, deep layer callosal neurons.

209 demonstrate a novel paradigm of cortical and callosal neuropathology in a mouse model of MS, perpetua

210 bstantially reduced compared with endogenous callosal OPCs 1 week after lesion and was lost on differ

211 f two anatomically distinguishable pathways, callosal or intracortical.

212 combined to examine the relationship between callosal organization and cortical activity across hemis

213 ovel evidence that individual differences in callosal organization are related to the extent of nondo

214 Wnt3 expression in the cingulate callosal pathfinding axons is developmentally regulated

215 y the induction of expression of Wnt3 by the callosal pathfinding neurons, which antagonize the inhib

216 cts of the functional characteristics of the callosal pathway in cat striate cortex.

217 loser to the spike-firing threshold than the callosal pathway.

218 ental disorder affecting thalamostriatal and callosal pathways, also present in the affected grandmot

219 ght exist between developing ipsilateral and callosal pathways.

220 ient involving the geniculo-cortical and the callosal pathways.

221 he extent to which development of the visual callosal pattern depends on retinal influences, and expl

222 tion at P20 had no significant effect on the callosal pattern, but it still caused a reduction in the

223 We studied the mature callosal patterns in normal ferrets and in ferrets bilat

224 Callosal patterns were revealed in tangential sections f

225 which the eyes influence the development of callosal patterns, but not the size of visual cortex, en

226 ate the existence and extent of cortical and callosal plasticity in these subjects.

227 ment of retrograde labeling of NeuN-positive callosal projecting neurons and reduction in the labelli

228 d stripping of synaptic proteins in cortical callosal projecting neurons.

229 ay a critical role in the acquisition of the callosal projection fate in layer 5.

230 regulates a decision between subcortical vs. callosal projection neuron fates.

231 vidual neurons adopt either a subcortical or callosal projection neuron identity at early times durin

232 Callosal projection neurons (CPN) are a diverse populati

233 Callosal projection neurons (CPN) connect the cerebral h

234 dendritic complexity of Mecp2-null cortical callosal projection neurons (CPN), and that NF-kappaB si

235 e molecular development and heterogeneity of callosal projection neurons (CPN), cortical commissural

236 send projections away from the cerebrum, and callosal projection neurons (CPN), which send projection

237 ubpopulations within the broad population of callosal projection neurons (CPN), whose axons connect t

238 vo lineage reprogramming of layer 2/3 (L2/3) callosal projection neurons (CPNs) into induced corticof

239 S1) cortex and postnatal day 3 (P3) purified callosal projection neurons (CPNs) with regard to neurot

240 populations of cortical projection neurons: callosal projection neurons and corticotectal projection

241 ex can be classified into two major classes: callosal projection neurons and long-range subcortical n

242 Fezf2(-/-) neurons adopt the fate of callosal projection neurons as assessed by their axonal

243 projection neurons and their replacement by callosal projection neurons cause distinctly abnormal la

244 anglion neurons, retinal ganglion cells, and callosal projection neurons during axon growth.

245 sion of exogenous Tubb2b-E421K in developing callosal projection neurons is sufficient to perturb hom

246 ther of CDO (Boc), is expressed in local and callosal projection neurons of layer II/III that synapse

247 ons in layer 5A and corticocortical neurons (callosal projection neurons similar to corticostriatal n

248 ularly subcategorize distinct populations of callosal projection neurons, often located in distinct s

249 n the early specification of subcerebral and callosal projection neurons, progressively increases aft

250 re expressed in lower cortical layers and in callosal projection neurons.

251 s in YFP(J16) mice cortex were identified as callosal projection neurons.

252 ions --> FS-PARV --> CCort) or facilitation (callosal projections --> CCol) of projecting neurons in

253 uits underlying either callosal suppression (callosal projections --> FS-PARV --> CCort) or facilitat

254 n in vitro, whereas Hsc70 activity supported callosal projections and radial neuronal migration in th

255 the neuronal microcircuits recruited by the callosal projections are unknown.

256 er, retina input specifies the topography of callosal projections by postnatal day (P)6.

257 te that during periods of acoustic exposure, callosal projections emanating from core auditory areas

258 d circuit mapping (CRACM), to map long-range callosal projections from layer (L) 2/3 of the somatosen

259 eafness, there was a significant decrease in callosal projections from the contralateral PAF.

260 In normal rats callosal projections in striate cortex connect retinotop

261 Studies of callosal projections in striate cortex show that the ret

262 We found that callosal projections suppress the activity of CCort pyra

263 his study, the role of the EphA subfamily in callosal projections was investigated using transgenic m

264 bility of the DTI-FT measurements, occipital-callosal projections were estimated from each subject's

265 mutual repression to produce subcortical or callosal projections.

266 in the thalamocortical, corticothalamic, and callosal projections.

267 opy (FA) and higher mean diffusivity (MD) in callosal regions and fibre bundles coursing through the

268 The callosal regions were differentially affected by alcohol

269 re area occupied by myelinated axons in both callosal regions.

270 Neither M1 inactivation nor callosal section changed contralateral response threshol

271 ximately 2 SD FA and MD abnormalities in the callosal sectors and fibres, abnormalities that were mor

272 ange, areas of restricted diffusion, diffuse callosal signal change, and atrophy and hyperintensity o

273 wer FA in the right posterior cingulum, left callosal splenium, right inferior fronto-occipital fasci

274 Two patients with anterior callosal strokes bisected lines to the left of midline w

275 sociation between antisocial personality and callosal structural abnormalities.

276 he effects of age and sex, whereas posterior callosal structure was associated with facilitation proc

277 ndicate the following dissociation: anterior callosal structure was associated with inhibitory proces

278 differs across individuals as a function of callosal structure, supporting a role for the corpus cal

279 the smaller area of each of the fiber-based callosal subdivisions.

280 Here the size of callosal subregions and area occupied by myelin were exa

281 The absolute size of callosal subregions differed between preterm and full-te

282 unknown cortical circuits underlying either callosal suppression (callosal projections --> FS-PARV -

283 grity, particularly in the fronto-limbic and callosal systems.

284 losal length (P =.002), a 15.3% reduction in callosal thickness (P =.04), and increased functional in

285 The temporally distinct changes in callosal thickness are likely to be a consequence of var

286 Except for the rostrum in females, callosal thickness increased across the whole surface, w

287 r to P4, is sufficient for specifying normal callosal topography.

288 left temporo-parietal areas and in posterior callosal tracts.

289 recording period indicating that the corpus callosal transection did not hinder these remote propaga

290 A separate group of animals underwent corpus callosal transection prior to electrocorticography (ECoG

291 is effect was not found in animals with both callosal transections and unilateral lesions.

292 the sensorimotor cortex (FLsmc) in rats, or callosal transections, cause neurons of the opposite mot

293 ions, or unilateral lesions, with or without callosal transections.

294 ried out auditory and visual tasks requiring callosal transfer with nine very preterm subjects with c

295 nsiderable delay, these progenitors generate callosal upper-layer neurons and glia.

296 arriers, presence of decreased white matter, callosal volume, and/or increased ventricle size was ass

297 Larger callosal volumes were associated with affective and inte

298 ontrols showed a 22.6% increase in estimated callosal white matter volume (P<.001), a 6.9% increase i

299 ymmetry and the connecting, interhemispheric callosal white matter was also investigated; minicolumn

300 g suggest that microstructural properties of callosal white matter, which includes myelination and ax